| + |
AKT1 | down-regulates 
phosphorylation
|
NR3C1 |
0.497 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252543 |
Ser134 |
ANLNRSTsVPENPKS |
Homo sapiens |
Acute Lymphoblastic Leukemia Cell |
| pmid |
sentence |
| 24291004 |
Akt1 impairs glucocorticoid-induced gene expression by direct phosphorylation of nr3c1 at position s134 and blocking glucocorticoid-induced nr3c1 translocation to the nucleus |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Adipogenesis |
| + |
AKT | down-regulates
phosphorylation
|
NR3C1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236216 |
Ser134 |
ANLNRSTsVPENPKS |
Homo sapiens |
Acute Lymphoblastic Leukemia Cell |
| pmid |
sentence |
| 24291004 |
Akt1 impairs glucocorticoid-induced gene expression by direct phosphorylation of nr3c1 at position s134 and blocking glucocorticoid-induced nr3c1 translocation to the nucleus |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SGK1 | up-regulates activity 
phosphorylation
|
NR3C1 |
0.473 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251669 |
Ser203 |
DLEFSSGsPGKETNE |
Homo sapiens |
|
| pmid |
sentence |
| 23650397 |
SGK1 also potentiated and maintained GR activation in the presence of cortisol, and even after cortisol withdrawal, by increasing GR phosphorylation and GR nuclear translocation|Having demonstrated that SGK1 mediates the cortisol-induced increase in GR phosphorylation at the S203 and S211 phospho-sites, which enhance GR nuclear translocation, but not at the S226 site, which inhibits nuclear translocation |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251670 |
Ser211 |
PGKETNEsPWRSDLL |
Homo sapiens |
|
| pmid |
sentence |
| 23650397 |
SGK1 also potentiated and maintained GR activation in the presence of cortisol, and even after cortisol withdrawal, by increasing GR phosphorylation and GR nuclear translocation|Having demonstrated that SGK1 mediates the cortisol-induced increase in GR phosphorylation at the S203 and S211 phospho-sites, which enhance GR nuclear translocation, but not at the S226 site, which inhibits nuclear translocation |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
CDK5 | down-regulates activity
phosphorylation
|
NR3C1 |
0.464 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-154401 |
Ser203 |
DLEFSSGsPGKETNE |
Homo sapiens |
|
| pmid |
sentence |
| 17440046 |
Cdk5 phosphorylated gr at multiple serines, including ser203 and ser211 of its n-terminal domain, and suppressed the transcriptional activity of this receptor on glucocorticoid-responsive promoters by attenuating attraction of transcriptional cofactors to dna.| the effect of CDK5 on GR-induced transcriptional activity is specific to gene promoter, and possibly, to tissue |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-154405 |
Ser211 |
PGKETNEsPWRSDLL |
Homo sapiens |
|
| pmid |
sentence |
| 17440046 |
Cdk5 phosphorylated gr at multiple serines, including ser203 and ser211 of its n-terminal domain, and suppressed the transcriptional activity of this receptor on glucocorticoid-responsive promoters by attenuating attraction of transcriptional cofactors to dna.| the effect of CDK5 on GR-induced transcriptional activity is specific to gene promoter, and possibly, to tissue |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
CDK2 | up-regulates activity
phosphorylation
|
NR3C1 |
0.296 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249426 |
Ser203 |
DLEFSSGsPGKETNE |
in vitro |
|
| pmid |
sentence |
| 9199329 |
Cyclin-dependent kinase (CDK) and mitogen-activated protein kinase (MAPK) phosphorylate the rat glucocorticoid receptor in vitro at distinct sites that together correspond to the major phosphorylated receptor residues observed in vivo; MAPK phosphorylates receptor residues threonine 171 and serine 246, whereas multiple CDK complexes modify serines 224 and 232.|MAPKs and CDKs exert opposite effects on receptor transcriptional enhancement. From our results, we speculate that activators of the MAPK pathway, such as growth factors, insulin, and certain oncoproteins, or inhibitors of CDK function, such as tumor growth factor beta (TGF_), p21, and p27, might attenuate receptor-induced transcrip- tional responses. In contrast, negative regulators of MAPK, such as pKA, as well as activators of CDK, such as the cyclins or CAKs, should potentiate receptor action. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249427 |
Ser211 |
PGKETNEsPWRSDLL |
in vitro |
|
| pmid |
sentence |
| 9199329 |
Cyclin-dependent kinase (CDK) and mitogen-activated protein kinase (MAPK) phosphorylate the rat glucocorticoid receptor in vitro at distinct sites that together correspond to the major phosphorylated receptor residues observed in vivo; MAPK phosphorylates receptor residues threonine 171 and serine 246, whereas multiple CDK complexes modify serines 224 and 232.|MAPKs and CDKs exert opposite effects on receptor transcriptional enhancement. From our results, we speculate that activators of the MAPK pathway, such as growth factors, insulin, and certain oncoproteins, or inhibitors of CDK function, such as tumor growth factor beta (TGF_), p21, and p27, might attenuate receptor-induced transcrip- tional responses. In contrast, negative regulators of MAPK, such as pKA, as well as activators of CDK, such as the cyclins or CAKs, should potentiate receptor action. |
|
| Publications: |
2 |
Organism: |
In Vitro |
| Pathways: | Adipogenesis |
| + |
MAPK14 | up-regulates
phosphorylation
|
NR3C1 |
0.495 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255952 |
Ser211 |
PGKETNEsPWRSDLL |
Mus musculus |
|
| pmid |
sentence |
| 20660302 |
We demonstrate here that AMPK differentially modulates glucocorticoid action by phosphorylating the human GR at serine 211 indirectly through the activation of p38 MAPK |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-135198 |
Ser211 |
PGKETNEsPWRSDLL |
Homo sapiens |
|
| pmid |
sentence |
| 15817653 |
We found serine 211 of the human gr to be a substrate for p38 mapk both in vitro and intracellularly. Mutation of this site to alanine greatly diminished gr-driven gene transcription and apoptosis. |
|
| Publications: |
2 |
Organism: |
Mus Musculus, Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
PPP5C | down-regulates activity
dephosphorylation
|
NR3C1 |
0.525 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248538 |
Ser211 |
PGKETNEsPWRSDLL |
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 19586900 |
Estrogen inhibits glucocorticoid action via protein phosphatase 5 (PP5)-mediated glucocorticoid receptor dephosphorylation.|Inhibition of GR phosphorylation at Ser-211 is associated with decreased nuclear retention of GR and decreased gene transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK3 | down-regulates
phosphorylation
|
NR3C1 |
0.527 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-154409 |
Ser226 |
IDENCLLsPLAGEDD |
in vitro |
|
| pmid |
sentence |
| 9199329 |
Cyclin-dependent kinase (CDK) and mitogen-activated protein kinase (MAPK) phosphorylate the rat glucocorticoid receptor in vitro at distinct sites that together correspond to the major phosphorylated receptor residues observed in vivo; MAPK phosphorylates receptor residues threonine 171 and serine 246, whereas multiple CDK complexes modify serines 224 and 232.|MAPKs and CDKs exert opposite effects on receptor transcriptional enhancement. From our results, we speculate that activators of the MAPK pathway, such as growth factors, insulin, and certain oncoproteins, or inhibitors of CDK function, such as tumor growth factor beta (TGF_), p21, and p27, might attenuate receptor-induced transcrip- tional responses. In contrast, negative regulators of MAPK, such as pKA, as well as activators of CDK, such as the cyclins or CAKs, should potentiate receptor action. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
MAPK1 | down-regulates activity
phosphorylation
|
NR3C1 |
0.61 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249428 |
Ser226 |
IDENCLLsPLAGEDD |
in vitro |
|
| pmid |
sentence |
| 9199329 |
Cyclin-dependent kinase (CDK) and mitogen-activated protein kinase (MAPK) phosphorylate the rat glucocorticoid receptor in vitro at distinct sites that together correspond to the major phosphorylated receptor residues observed in vivo; MAPK phosphorylates receptor residues threonine 171 and serine 246, whereas multiple CDK complexes modify serines 224 and 232.|MAPKs and CDKs exert opposite effects on receptor transcriptional enhancement. From our results, we speculate that activators of the MAPK pathway, such as growth factors, insulin, and certain oncoproteins, or inhibitors of CDK function, such as tumor growth factor beta (TGF_), p21, and p27, might attenuate receptor-induced transcrip- tional responses. In contrast, negative regulators of MAPK, such as pKA, as well as activators of CDK, such as the cyclins or CAKs, should potentiate receptor action. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
ERK1/2 | down-regulates
phosphorylation
|
NR3C1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-93554 |
Ser226 |
IDENCLLsPLAGEDD |
in vitro |
|
| pmid |
sentence |
| 9199329 |
Cyclin-dependent kinase (CDK) and mitogen-activated protein kinase (MAPK) phosphorylate the rat glucocorticoid receptor in vitro at distinct sites that together correspond to the major phosphorylated receptor residues observed in vivo; MAPK phosphorylates receptor residues threonine 171 and serine 246, whereas multiple CDK complexes modify serines 224 and 232.|MAPKs and CDKs exert opposite effects on receptor transcriptional enhancement. From our results, we speculate that activators of the MAPK pathway, such as growth factors, insulin, and certain oncoproteins, or inhibitors of CDK function, such as tumor growth factor beta (TGF_), p21, and p27, might attenuate receptor-induced transcrip- tional responses. In contrast, negative regulators of MAPK, such as pKA, as well as activators of CDK, such as the cyclins or CAKs, should potentiate receptor action. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | Adipogenesis |
| + |
MAPK8 | down-regulates
phosphorylation
|
NR3C1 |
0.626 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-93558 |
Ser226 |
IDENCLLsPLAGEDD |
Homo sapiens |
|
| pmid |
sentence |
| 12351702 |
Taken together, these findings suggest that jnk-mediated phosphorylation of the gr-ser226 enhances gr nuclear export and may contribute to termination of gr-mediated transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
GSK3B | down-regulates activity
phosphorylation
|
NR3C1 |
0.525 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-181541 |
Ser404 |
SMRPDVSsPPSSSST |
Homo sapiens |
|
| pmid |
sentence |
| 18838540 |
We found hormone-dependent GR phosphorylation on serine 404 by GSK-3beta [ ]Cells expressing a GR that is incapable of GSK-3beta phosphorylation had a redirection of the global transcriptional response to hormone, including the activation of additional signaling pathways, in part due to the altered ability of unphosphorylatable GR to recruit transcriptional cofactors CBP/p300 and the p65 (RelA) subunit of NF-kappaB |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Adipogenesis |
| + |
PRKDC |
phosphorylation
|
NR3C1 |
0.354 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248965 |
Ser508 |
QQATTGVsQETSENP |
in vitro |
|
| pmid |
sentence |
| 9038175 |
Phosphorylation of the GR fusion protein by DNA-PK mapped to a single site, Ser-527. This site occurs adjacent the GR nuclear localization sequence between the DNA and ligand binding domains of GR, and thus its phosphorylation, if confirmed, has the potential to affect receptor function in vivo. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
PER2 |
0.483 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268049 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19805059 |
GR directly regulates transcription of circadian clock components in mouse and human primary MSCs. Per2, E4bp4, Per1, and Timeless rapidly respond to glucocorticoid stimulation. Primary glucocorticoid receptor (GR) target genes are those at which GR occupies a nearby genomic glucocorticoid response element (GRE) and regulates target gene transcription |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Circadian clock |
| + |
HSPA1A | down-regulates
binding
|
NR3C1 |
0.621 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251668 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21730050 |
Interestingly, FKBP51 forms complexes in mitochondria with the glucocorticoid receptor and the Hsp90/Hsp70-based chaperone heterocomplex |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates activity
relocalization
|
KAT2B |
0.533 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269233 |
|
|
|
|
| pmid |
sentence |
| 32917954 |
NR3C1 impaired GLI1 function by dynamically modulating the recruitment of PCAF acetyltransferase |
|
| Publications: |
1 |
| + |
6alpha-methylprednisolone | up-regulates
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251696 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 6749443 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251695 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9259419 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251697 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 1159081 |
|
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates quantity by expression 
transcriptional regulation
|
KLF15 |
0.383 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236212 |
|
|
Mus musculus |
MEF Cell |
| pmid |
sentence |
| 20956975 |
We identified glucocorticoid response element sites in the first intron of KLF15 by bioinformatical promoter analysis and confirmed their functional relevance by demonstrating GR interaction by chromatin immunoprecipitation |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
mifepristone | down-regulates activity
chemical inhibition
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258709 |
|
|
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 8282004 |
The sex steroid progesterone bound with an affinity (ki < 0.01 nM) even higher than that of aldosterone to the human mineralocorticoid receptor and effectively antagonized the effect of aldosterone via the human mineralocorticoid receptor in functional co-transfection assays. This indicates that progesterone has potent antimineralocorticoid properties, while its antiglucocorticoid effects were less pronounced. The partial agonistic activities of antihormones in this assay suggest a direct interaction of antihormone-receptor complexes with the response elements on the DNA. aldosterone shows a higher functional sensitivity for the human mineralocorticoid receptor than deoxycorticosterone (higher affinity) or cortisol (similar affinity). Moreover, the very high binding affinity of the human mineralocorticoid receptor for progesterone (k i < 0.0l nM) in combination with the very low agonistic activity indicates that progesterone may act as a potent human mineralocorticoid receptor antagonist that is even more effective than spironolactone (k~ = 5.7 nM), which displays no partial agonistic activity (fig. 4). |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
NR3C1 | up-regulates quantity
transcriptional regulation
|
FOXO3 |
0.425 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255759 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 22848740 |
We show that FOXO3 is an immediate early glucocorticoid receptor (GR) target, whose transcription is even further enhanced by conditions that mimic metabolic stress. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
prednisone | up-regulates
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251703 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9753485 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251706 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8143061 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251705 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 4188963 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251704 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 4344326 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251702 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 3930339 |
|
|
| Publications: |
5 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
CEBPA |
0.465 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256116 |
|
|
Mus musculus |
Preadipocyte Cell Line |
| pmid |
sentence |
| 27777311 |
We show that in addition, DEX-bound GR directly promotes the expression of adipogenic TFs, including C/EBPβ, Klf5, Klf9, and C/EBPα |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Adipogenesis |
| + |
CRTC2 | up-regulates activity
binding
|
NR3C1 |
0.298 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256101 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26652733 |
We show here that CRTC2 also functions as a coactivator for the glucocorticoid receptor (GR). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
TSC22D3 |
0.424 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253295 |
|
|
Mus musculus |
Thymocyte |
| pmid |
sentence |
| 9430225 |
In thymocytes and peripheral T cells, GILZ gene expression is induced by DEX |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
CEBPB |
0.47 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256117 |
|
|
Mus musculus |
Preadipocyte Cell Line |
| pmid |
sentence |
| 27777311 |
We show that in addition, DEX-bound GR directly promotes the expression of adipogenic TFs, including C/EBPβ, Klf5, Klf9, and C/EBPα. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Adipogenesis |
| + |
NR3C1 | up-regulates
binding
|
STAT5A |
0.544 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-44376 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8878484 |
We show here that the glucocorticoid receptor can act as a transcriptional co-activator for stat5 and enhance stat5-dependent transcription. Stat5 forms a complex with the gluco-corticoid receptor which binds to dna independently of the gre. This complex formation between stat5 and the glucocorticoid receptor diminishes the glucocorticoid response of a gre-con-taining promoter. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
budesonide | up-regulates
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251687 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11208622 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251688 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 6958488 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251689 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9657565 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251690 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9753485 |
|
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates quantity
transcriptional regulation
|
PPARG |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255963 |
|
|
Mus musculus |
3T3-L1 Cell |
| pmid |
sentence |
| 8754811 |
Induction of peroxisome proliferator-activated receptor gamma during the conversion of 3T3 fibroblasts into adipocytes is mediated by C/EBPbeta, C/EBPdelta, and glucocorticoids. The dose of DEX required to promote maximal expression of PPARg mRNA is approximately 10 nM, which is within the range of the Kd for the association of DEX with the glucocorticoid receptor in 3T3-L1 cells. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Adipogenesis, Circadian clock |
| + |
NR3C1 | up-regulates
|
NR3C2 |
0.525 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-85987 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11154266 |
These results indicate that functional interactions between the glucocorticoid and mineralocorticoid receptors in activating specific gene transcription are probably more complex than has been previously appreciated. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | down-regulates activity 
|
Gbeta |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269898 |
|
|
Mus musculus |
NIH-3T3 Cell |
| pmid |
sentence |
| 11742987 |
Both induction of MKP-1 expression and inhibition of its degradation are necessary for glucocorticoid-mediated inhibition of Erk-1/2 activation. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
NR3C1 | down-regulates activity
|
ERK1/2 |
0.621 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269920 |
|
|
Mus musculus |
NIH-3T3 Cell |
| pmid |
sentence |
| 11742987 |
Both induction of MKP-1 expression and inhibition of its degradation are necessary for glucocorticoid-mediated inhibition of Erk-1/2 activation. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Adipogenesis |
| + |
prednisolone | up-regulates
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251701 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8335191 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251700 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 13760840 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251698 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8342904 |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251699 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11777359 |
|
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
HES1 | down-regulates activity
|
NR3C1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253064 |
|
|
Homo sapiens |
U2-OS Cell |
| pmid |
sentence |
| 24300895 |
Altering the expression of HES1 did not obviously affect GR abundance (Figure 3A). However, genome-wide microarrays revealed that overexpression of HES1 resulted in inhibition of GR-mediated changes in the glucocorticoid regulated transcriptome, as compared to non-overexpressing controls |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | down-regulates quantity by repression
transcriptional regulation
|
ATP1B1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254864 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9694812 |
Together these data indicate that the 21-base pair sequence represents a true MRE/GRE and that optimal activation of the human Na/K-ATPase beta1 promoter is controlled by mineralocorticoid and glucocorticoid hormones. It appears that an interaction of MR with GR on the beta1 promoter effectively down-regulates transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates quantity
transcriptional regulation
|
G6P |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270258 |
|
|
Pongo pygmaeus |
HeLa Cell |
| pmid |
sentence |
| 26652733 |
Further, CRTC2 is required for the glucocorticoid-associated cooperative mRNA expression of the glucose-6-phosphatase, a rate-limiting enzyme for hepatic gluconeogenesis, by facilitating the attraction of GR and itself to its promoter region already occupied by CREB |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267792 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26652733 |
Further, CRTC2 is required for the glucocorticoid-associated cooperative mRNA expression of the glucose-6-phosphatase, a rate-limiting enzyme for hepatic gluconeogenesis, by facilitating the attraction of GR and itself to its promoter region already occupied by CREB |
|
| Publications: |
2 |
Organism: |
Pongo Pygmaeus, Homo Sapiens |
| + |
NR3C1 | down-regulates quantity by repression
transcriptional regulation
|
NR4A1 |
0.328 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-132251 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15591535 |
Our data suggest a mechanism for transrepression between two nuclear receptors, gr and ngfi-b. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | down-regulates activity
|
MAPK3 |
0.527 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251677 |
|
|
Mus musculus |
NIH-3T3 Cell |
| pmid |
sentence |
| 11742987 |
Both induction of MKP-1 expression and inhibition of its degradation are necessary for glucocorticoid-mediated inhibition of Erk-1/2 activation. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates
binding
|
HDAC1 |
0.455 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253057 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 18762022 |
The GR directly interferes with Hes1 promoter activity, triggering the recruitment of histone deacetylase (HDAC) activities to the Hes1 gene |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
KLF5 |
0.296 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256118 |
|
|
Mus musculus |
Preadipocyte Cell Line |
| pmid |
sentence |
| 27777311 |
We show that in addition, DEX-bound GR directly promotes the expression of adipogenic TFs, including C/EBPβ, Klf5, Klf9, and C/EBPα |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Adipogenesis |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
RXRA |
0.446 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-98102 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12573484 |
Physiological concentrations of glucocorticoids increase cellular cyp2c9 (and cyp3a5) but also car, rxr and pxr levels via a gr-mediated mechanism |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | down-regulates quantity by repression
transcriptional regulation
|
JUN |
0.735 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251679 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8639160 |
We have described how the receptor uses several means to achieve repression of the genes regulated by AP-1 and NF-KB proteins |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
cortisol | up-regulates activity
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258708 |
|
|
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 8282004 |
The sex steroid progesterone bound with an affinity (ki < 0.01 nM) even higher than that of aldosterone to the human mineralocorticoid receptor and effectively antagonized the effect of aldosterone via the human mineralocorticoid receptor in functional co-transfection assays. This indicates that progesterone has potent antimineralocorticoid properties, while its antiglucocorticoid effects were less pronounced. The partial agonistic activities of antihormones in this assay suggest a direct interaction of antihormone-receptor complexes with the response elements on the DNA. aldosterone shows a higher functional sensitivity for the human mineralocorticoid receptor than deoxycorticosterone (higher affinity) or cortisol (similar affinity). Moreover, the very high binding affinity of the human mineralocorticoid receptor for progesterone (k i < 0.0l nM) in combination with the very low agonistic activity indicates that progesterone may act as a potent human mineralocorticoid receptor antagonist that is even more effective than spironolactone (k~ = 5.7 nM), which displays no partial agonistic activity (fig. 4). |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
NR3C1 | down-regulates activity
|
MAPK8 |
0.626 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251676 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 11742987 |
GR-mediated inhibition of c-Jun N-terminal kinase (JNK) activity |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
budesonide | up-regulates activity
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253053 |
|
|
in vitro |
|
| pmid |
sentence |
| 9793625 |
Mometasone furoate (MF, CAS 83919-23-7, Sch 32088), budesonide (BUD, CAS 51372-29-3), fluticasone propionate (FP, CAS 80474-14-2), and triamcinolone acetonide (TA, CAS-76-25-5) are corticosteroids. All of the test compounds had a higher affinity for the recombinant glucocorticoid receptor than the reference glucocorticoid receptor ligand, dexamethasone (DEX, CAS 50-02-2). All compounds showed greater potency than dexamethasone in stimulating transcription of a synthetic target gene regulated by a glucocorticoid response element. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates quantity
transcriptional regulation
|
PCK1 |
0.368 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256107 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26652733 |
These results reveal that CRTC2 plays an essential role in the regulation of hepatic gluconeogenesis through coordinated regulation of the glucocorticoid/GR- and glucagon/CREB-signaling pathways on the key genes G6P and PEPCK. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253056 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 11069927 |
In the liver, glucocorticoids induce a 10-15-fold increase in the rate of transcription of the phosphoenolpyruvate carboxykinase (PEPCK) gene, which encodes a key gluconeogenic enzyme |
|
| Publications: |
2 |
Organism: |
Homo Sapiens, Rattus Norvegicus |
| + |
NR3C1 | form complex 
binding
|
NR3C1/STAT5A |
0.544 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-44373 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8878484 |
We show here that the glucocorticoid receptor can act as a transcriptional co-activator for stat5 and enhance stat5-dependent transcription. Stat5 forms a complex with the gluco-corticoid receptor which binds to dna independently of the gre. This complex formation between stat5 and the glucocorticoid receptor diminishes the glucocorticoid response of a gre-con-taining promoter. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates
binding
|
LCK |
0.361 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251685 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16888650 |
The present study shows that the GC receptor is part of a TCR-linked multiprotein complex containing heat-shock protein (HSP)90, LCK and FYN, which is essential for TCR-dependent LCK/FYN activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
FKBP5 | down-regulates
binding
|
NR3C1 |
0.739 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251666 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25790864 |
When not associated with glucocorticoids, glucocorticoid receptors are predominantly found in the cytoplasm as part of a multimeric molecular chaperone complex that includes several heat shock proteins (HSPs), such as HSP70 and HSP90, the HSP90_binding protein p23 (also known as PTGES3) and proteins that help to bind HSP90 such as FK506_binding protein 5 (FKBP5). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
NR2F2 |
0.356 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-121422 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14739255 |
Gralpha, but not grbeta, enhanced coup-tfii-induced transactivation of the simple coup-tfii-responsive 7alpha-hydroxylase promoter through the transcriptional activity of its activation function-1 domain, whereas coup-tfii repressed gralpha-induced transactivation of the glucocorticoid-responsive promoter by attracting the silencing mediator for retinoid and thyroid hormone receptors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
TRIM63 |
0.336 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254992 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 18612045 |
Consistent with these findings, DEX-induced upregulation of MuRF1 is significantly attenuated in mice expressing a homodimerization-deficient GR despite no effect on the degree of muscle loss in these mice vs. their wild-type counterparts. Finally, chromatin immunoprecipitation analysis reveals that both GR and FOXO1 bind to the endogenous MuRF1 promoter in C(2)C(12) myotubes, and IGF-I inhibition of DEX-induced MuRF1 expression correlates with the loss of FOXO1 binding. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
NFIL3 |
0.301 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268051 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19805059 |
GR directly regulates transcription of circadian clock components in mouse and human primary MSCs. Per2, E4bp4, Per1, and Timeless rapidly respond to glucocorticoid stimulation. Primary glucocorticoid receptor (GR) target genes are those at which GR occupies a nearby genomic glucocorticoid response element (GRE) and regulates target gene transcription |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Circadian clock |
| + |
NCOA2 | up-regulates activity
binding
|
NR3C1 |
0.833 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256095 |
|
|
Mus musculus |
Macrophage |
| pmid |
sentence |
| 29170386 |
Here we report that GRIP1 loss in macrophages attenuates glucocorticoid induction of several anti-inflammatory targets, and that GC treatment of quiescent macrophages globally directs GRIP1 toward GR binding sites dominated by palindromic GC response elements (GRE), suggesting a non-redundant GRIP1 function as a GR coactivator. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
PPARG |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255753 |
|
|
Mus musculus |
3T3-L1 Cell |
| pmid |
sentence |
| 10649448 |
The dose of DEX required to promote maximal expression of PPARg mRNA is approximately 10 nM, which is within the range of the Kd for the association of DEX with the glucocorticoid receptor in 3T3-L1 cells |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256120 |
|
|
Mus musculus |
Preadipocyte Cell Line |
| pmid |
sentence |
| 27777311 |
We observed GR binding on or near Cebpβ, Cebpδ, Klf5, Klf9, Cebpα, and Pparγ gene loci at 4 h but not at 0 h of adipogenesis. Thus, at least one of the mechanisms by which GR promotes adipogenesis in culture is by directly activating the expression of multiple adipogenic TFs. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250561 |
|
|
Mus musculus |
3T3-L1 Cell |
| pmid |
sentence |
| 11279134 |
The differentiation of 3T3-L1 preadipocytes is regulated in part by a cascade of transcriptional events involving activation of the CCAAT/enhancer-binding proteins (C/EBPs) and peroxisome proliferator-activated receptor gamma (PPARgamma) by dexamethasone (DEX), 3-isobutyl-1-methylxanthine (MIX), and insulin |
|
| Publications: |
3 |
Organism: |
Mus Musculus |
| Pathways: | Adipogenesis, Circadian clock |
| + |
NR2F2 | up-regulates quantity by expression
transcriptional regulation
|
NR3C1 |
0.356 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-121419 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14739255 |
Gralpha, but not grbeta, enhanced coup-tfii-induced transactivation of the simple coup-tfii-responsive 7alpha-hydroxylase promoter through the transcriptional activity of its activation function-1 domain, whereas coup-tfii repressed gralpha-induced transactivation of the glucocorticoid-responsive promoter by attracting the silencing mediator for retinoid and thyroid hormone receptors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates quantity
|
DUSP1 |
0.567 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253546 |
|
|
Mus musculus |
NIH-3T3 Cell |
| pmid |
sentence |
| 11742987 |
Glucocorticoids inhibit MAP kinase via increased expression and decreased degradation of MKP-1|Both induction of MKP-1 expression and inhibition of its degradation are necessary for glucocorticoid-mediated inhibition of Erk-1/2 activation. In NIH-3T3 fibroblasts, although glucocorticoids up-regulate the MKP-1 level, they do not attenuate the proteasomal degradation of this protein and consequently they are unable to inhibit Erk-1/2 activity. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
NR3C1 | down-regulates quantity by repression
transcriptional regulation
|
NFKB1 |
0.586 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251680 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8639160 |
We have described how the receptor uses several means to achieve repression of the genes regulated by AP-1 and NF-KB proteins |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates quantity
transcriptional regulation
|
IRAK3 |
0.368 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259287 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25585690 |
We show that glucocorticoids and non-typeable Haemophilus influenzae synergistically upregulate IRAK-M expression via mutually and synergistically enhancing p65 and glucocorticoid receptor binding to the IRAK-M promoter |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HSP90AA1 | down-regulates
binding
|
NR3C1 |
0.727 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251667 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21511880 |
We report the crucial underlying role of the intranuclear heat shock protein 90 molecular chaperone complex in pulsatile GR regulation. Pharmacological interference of heat shock protein 90 (HSP90) with geldanamycin during the intranuclear chaperone cycle completely ablated GR's cyclical activity, cyclical cAMP response element-binding protein (CREB) binding protein (CBP)/p300 recruitment, and the associated cyclical acetylation at the promoter region. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
UGT1A1 |
0.286 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254439 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18172616 |
This study indicates that hepatocyte nuclear factor 1alpha (HNF1alpha) bound to the proximal promoter motif not only enhances the basal reporter activity of UGT1A1, including the distal (-3570/-3180) and proximal (-165/-1) regions, but also influences the transcriptional regulation of UGT1A1 by CAR, PXR, GR, and AhR to markedly enhance reporter activities. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
NFKBIA |
0.333 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255688 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 7569975 |
Here it is shown that the synthetic glucocorticoid dexamethasone induces the transcription of the IKBc gene, which results in an increased rate of IKBa protein synthesis |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
cortisone | up-regulates
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251691 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14817168 |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | down-regulates
|
Inflammation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257599 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25910399 |
Glucocorticoids (GCs) are the most commonly used anti-inflammatory agents to treat inflammatory and immune diseases [.. }The dogma that transrepression of genes, by tethering of the glucocorticoid receptor (GR) to DNA-bound pro-inflammatory transcription factors, is the main anti-inflammatory mechanism, is now challenged. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
CLOCK | down-regulates quantity by repression
transcriptional regulation
|
NR3C1 |
0.419 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253699 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21164265 |
We recently reported that the basic helix-loop- helix transcription factor Clock, which is a histone acetyltransferase and a central component of the self-oscillating transcription factor loop that generates circadian rhythms, represses GR transcriptional activity by acetylating lysine residues within the 'lysine cluster' located in the hinge region of the receptor. This Clock-mediated repression of GR transcriptional activity oscillates in inverse phase to the HPA axis, acting as a target tissue counter-regulatory mechanism to the diurnally fluctuating circulating glucocorticoids. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Circadian clock |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
TIMELESS |
0.255 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268052 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19805059 |
GR directly regulates transcription of circadian clock components in mouse and human primary MSCs. Per2, E4bp4, Per1, and Timeless rapidly respond to glucocorticoid stimulation. Primary glucocorticoid receptor (GR) target genes are those at which GR occupies a nearby genomic glucocorticoid response element (GRE) and regulates target gene transcription |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Circadian clock |
| + |
dehydroepiandrosterone | up-regulates
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251707 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9489820 |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates activity
|
Inflammation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266901 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25910399 |
Glucocorticoids (GCs) are the most commonly used anti-inflammatory agents to treat inflammatory and immune diseases [.. }The dogma that transrepression of genes, by tethering of the glucocorticoid receptor (GR) to DNA-bound pro-inflammatory transcription factors, is the main anti-inflammatory mechanism, is now challenged. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
glucocorticoid | up-regulates activity
binding
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268048 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18049904 |
Glucocorticoid action in cells is mediated by a specific receptor protein, the glucocorticoid receptor (GR). GR is a member of a superfamily of ligand-inducible transcription factors that control a variety of physiological functions; such as, metabolism, development, and reproduction. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Circadian clock |
| + |
NR4A1 | down-regulates quantity by repression
transcriptional regulation
|
NR3C1 |
0.328 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-132312 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15591535 |
Our data suggest a mechanism for transrepression between two nuclear receptors, gr and ngfi-b. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
KLF9 |
0.327 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256119 |
|
|
Mus musculus |
Preadipocyte Cell Line |
| pmid |
sentence |
| 27777311 |
We show that in addition, DEX-bound GR directly promotes the expression of adipogenic TFs, including C/EBPβ, Klf5, Klf9, and C/EBPα |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
NR3C1 | up-regulates activity
binding
|
CEBPB |
0.47 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250566 |
|
|
Mus musculus |
3T3-L1 Cell |
| pmid |
sentence |
| 11279134 |
The differentiation of 3T3-L1 preadipocytes is regulated in part by a cascade of transcriptional events involving activation of the CCAAT/enhancer-binding proteins (C/EBPs) and peroxisome proliferator-activated receptor gamma (PPARgamma) by dexamethasone (DEX), 3-isobutyl-1-methylxanthine (MIX), and insulin |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251655 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 9428795 |
We have shown that one of the functions of the GR to activate transcription of the AGP gene is to recruit C/EBPbeta and to maintain it bound at its target DNA sequences (SRU) |
|
| Publications: |
2 |
Organism: |
Mus Musculus, Rattus Norvegicus |
| Pathways: | Adipogenesis |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
CEBPA |
0.465 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235346 |
|
|
Mus musculus |
3T3-L1 Cell |
| pmid |
sentence |
| 11279134 |
The differentiation of 3T3-L1 preadipocytes is regulated in part by a cascade of transcriptional events involving activation of the CCAAT/enhancer-binding proteins (C/EBPs) and peroxisome proliferator-activated receptor gamma (PPARgamma) by dexamethasone (DEX), 3-isobutyl-1-methylxanthine (MIX), and insulin |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Adipogenesis |
| + |
HES1 | down-regulates quantity by repression
transcriptional regulation
|
NR3C1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251674 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19129776 |
HES1 binding to the promoter of the NC3C1 gene inhibits its expression and results in insufficient production of the encoded glucocorticoid receptor- rendering these cells resistant to treatment with dexamethasone |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Gbeta | down-regulates
phosphorylation
|
NR3C1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270098 |
|
|
in vitro |
|
| pmid |
sentence |
| 9199329 |
Cyclin-dependent kinase (CDK) and mitogen-activated protein kinase (MAPK) phosphorylate the rat glucocorticoid receptor in vitro at distinct sites that together correspond to the major phosphorylated receptor residues observed in vivo; MAPK phosphorylates receptor residues threonine 171 and serine 246, whereas multiple CDK complexes modify serines 224 and 232.|MAPKs and CDKs exert opposite effects on receptor transcriptional enhancement. From our results, we speculate that activators of the MAPK pathway, such as growth factors, insulin, and certain oncoproteins, or inhibitors of CDK function, such as tumor growth factor beta (TGF_), p21, and p27, might attenuate receptor-induced transcrip- tional responses. In contrast, negative regulators of MAPK, such as pKA, as well as activators of CDK, such as the cyclins or CAKs, should potentiate receptor action. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
dexamethasone | up-regulates
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251694 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27660409 |
They differ according to their glucocorticoid-receptor binding affinities (dexamethasone > triamcinolone > fluocinolone) and their lipophilicity (triamcinolone > fluocinolone > dexamethasone), characteristics that may partially explain their relative potencies |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-168562 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20956975 |
Glucocorticoids, such as dexamethasone, have been used as in vitro inducers of adipogenesis. However, the roles of the glucocorticoid receptor (gr) in adipogenesis have not been well characterized yet. Here, we show that inhibition of gr activity using the gr antagonist ru486 prevents human mesenchymal stem cell and mouse embryonic fibroblast (mef) differentiation into adipocytes |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | down-regulates quantity by repression
transcriptional regulation
|
NR4A2 |
0.31 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-132254 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15591535 |
We now show that the other nur factors, nurr1 and nor-1, are also subject to antagonism by gr and that this transrepression appears to involve direct protein-protein interactions between the dbds of gr and nur factors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
NCOA1 |
0.763 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251682 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9590696 |
Transactivation of these templates depends on the association of the GR with co-activators such as SRC-1/NcoA1, GRIP-1/TIF-2/NcoA2 and p300/CBP. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
PTMS | up-regulates quantity by expression
transcriptional regulation
|
NR3C1 |
0.332 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268460 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 16150697 |
Macromolecular translocation inhibitor II (MTI-II), which was first identified as an in vitro inhibitor of binding between the highly purified glucocorticoid receptor (GR) and isolated nuclei, is an 11.5-kDa Zn2+-binding protein that is also known as ZnBP or parathymosin. MTI-II Enhances GR-dependent Transcription through Its Acidic Domain. MTI-II Enhances GR-dependent Transcription in Cooperation with SRC-1 and p300 in Vivo. CBP and p300 Coprecipitate with MTI-II in a Glucocorticoid Hormone-dependent Manner |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
betamethasone | up-regulates
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251686 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17561562 |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates quantity
transcriptional regulation
|
CEBPD |
0.32 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251648 |
|
|
Mus musculus |
3T3-L1 Cell |
| pmid |
sentence |
| 1840554 |
The expression levels of both C/EBPB and C/EBPD are increased dramatically during the time of hormonal stimulation (see Fig. 8). Furthermore, the C/EBPB- and C/EBPD encoding genes are activated directly by adipogenic hormones |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253061 |
|
|
Mus musculus |
3T3-L1 Cell |
| pmid |
sentence |
| 10649448 |
We conclude that glucocorticoid-induced adipogenesis from bone marrow stromal cells is mediated through a reaction cascade in which dexamethasone transcriptionally activates C/EBPδ; C/EBPδ then binds to PPARγ2 promoter and transactivates PPARγ2 gene expression. |
|
| Publications: |
2 |
Organism: |
Mus Musculus |
| Pathways: | Adipogenesis |
| + |
NR3C1 | up-regulates
binding
|
CAV1 |
0.387 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251683 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23339905 |
He mGR appears to reside in caveolae and its association with caveolin-1 (Cav-1) was clearly detected in two of the four cell lines investigated using double recognition proximity ligation assay. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates quantity
transcriptional regulation
|
SGK1 |
0.473 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255926 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 15793248 |
We show here that dexamethasone upregulates transcription and expression of the serum- and glucocorticoid-inducible kinase 1 (SGK1) in insulin-secreting cells, an effect reversed by mifepristone (RU486), an antagonist of the nuclear glucocorticoid receptor. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
dexamethasone | up-regulates activity
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258711 |
|
|
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 8282004 |
The sex steroid progesterone bound with an affinity (ki < 0.01 nM) even higher than that of aldosterone to the human mineralocorticoid receptor and effectively antagonized the effect of aldosterone via the human mineralocorticoid receptor in functional co-transfection assays. This indicates that progesterone has potent antimineralocorticoid properties, while its antiglucocorticoid effects were less pronounced. The partial agonistic activities of antihormones in this assay suggest a direct interaction of antihormone-receptor complexes with the response elements on the DNA. aldosterone shows a higher functional sensitivity for the human mineralocorticoid receptor than deoxycorticosterone (higher affinity) or cortisol (similar affinity). Moreover, the very high binding affinity of the human mineralocorticoid receptor for progesterone (k i < 0.0l nM) in combination with the very low agonistic activity indicates that progesterone may act as a potent human mineralocorticoid receptor antagonist that is even more effective than spironolactone (k~ = 5.7 nM), which displays no partial agonistic activity (fig. 4). |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | down-regulates quantity by repression
transcriptional regulation
|
TDO2 |
0.344 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268995 |
|
|
|
|
| pmid |
sentence |
| 16272140 |
Repression of GR-mediated expression of the tryptophan oxygenase gene by the SWI/SNF complex during liver development. |
|
| Publications: |
1 |
| + |
Difluprednate | up-regulates activity
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257886 |
|
|
in vitro |
|
| pmid |
sentence |
| 21182429 |
BMP had the highest K(i) value (8.4 × 10(-8) nmol/L), whereas DFB had the lowest (6.1 × 10(-11) nmol/L). The GCRBA of DFBA was intermediate to these 2 values (7.8 × 10(-10) nmol/L). |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
clobetasol | up-regulates activity
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269217 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 4594577 |
The clinical evaluation of a new topical corticosteroid, clobetasol propionate. An international controlled trial. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates quantity
transcriptional regulation
|
G6PC1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256104 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26652733 |
Further, CRTC2 is required for the glucocorticoid-associated cooperative mRNA expression of the glucose-6-phosphatase, a rate-limiting enzyme for hepatic gluconeogenesis, by facilitating the attraction of GR and itself to its promoter region already occupied by CREB |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AR | down-regulates quantity by repression
binding
|
NR3C1 |
0.53 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-48513 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9162033 |
Androgen and glucocorticoid receptor heterodimer formation. A possible mechanism for mutual inhibition of transcriptional activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | down-regulates activity
|
MAPK1 |
0.61 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251678 |
|
|
Mus musculus |
NIH-3T3 Cell |
| pmid |
sentence |
| 11742987 |
Glucocorticoids inhibit MAP kinase via increased expression and decreased degradation of MKP-1|Both induction of MKP-1 expression and inhibition of its degradation are necessary for glucocorticoid-mediated inhibition of Erk-1/2 activation. In NIH-3T3 fibroblasts, although glucocorticoids up-regulate the MKP-1 level, they do not attenuate the proteasomal degradation of this protein and consequently they are unable to inhibit Erk-1/2 activity. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NR3C1 | down-regulates activity
binding
|
AR |
0.53 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-48516 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9162033 |
Androgen and glucocorticoid receptor heterodimer formation. A possible mechanism for mutual inhibition of transcriptional activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PPP1CA | up-regulates activity
dephosphorylation
|
NR3C1 |
0.295 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277161 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32585168 |
The current study assessed whether PP1\u03b1 can stimulate GR function and tested two different hypotheses: First, that PP1\u03b1 regulates GR activity through suppression of MDM2 activity by dephosphorylating it at Ser166, thereby reducing the MDM2-mediated ubiquitination of GR and the subsequent proteasomal degradation of the receptor, as shown for the MR and AR ( xref ; xref ); and second, that PP1\u03b1 directly dephosphorylates the GR at a particular site to relieve functional repression as demonstrated for PP2A and PP5 ( xref ; xref ; xref ).|The involvement of GR-Ser211 phosphorylation supports the assumption that altered subcellular trafficking is a mechanism less likely contributing to the PP1\u03b1-dependent GR activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
11-deoxycorticosterone | up-regulates activity
chemical activation
|
NR3C1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258713 |
|
|
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 8282004 |
The sex steroid progesterone bound with an affinity (ki < 0.01 nM) even higher than that of aldosterone to the human mineralocorticoid receptor and effectively antagonized the effect of aldosterone via the human mineralocorticoid receptor in functional co-transfection assays. This indicates that progesterone has potent antimineralocorticoid properties, while its antiglucocorticoid effects were less pronounced. The partial agonistic activities of antihormones in this assay suggest a direct interaction of antihormone-receptor complexes with the response elements on the DNA. aldosterone shows a higher functional sensitivity for the human mineralocorticoid receptor than deoxycorticosterone (higher affinity) or cortisol (similar affinity). Moreover, the very high binding affinity of the human mineralocorticoid receptor for progesterone (k i < 0.0l nM) in combination with the very low agonistic activity indicates that progesterone may act as a potent human mineralocorticoid receptor antagonist that is even more effective than spironolactone (k~ = 5.7 nM), which displays no partial agonistic activity (fig. 4). |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
NR3C1 | down-regulates activity
|
MAPK14 |
0.495 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251675 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 11742987 |
The MAP kinase p38 is also a target for negative regulation by glucocorticoids |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
PELP1 | up-regulates quantity by expression
transcriptional regulation
|
NR3C1 |
0.537 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251681 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18682536 |
MNAR functionally interacts with both NH2- and COOH-terminal GR domains to modulate transactivation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
PER1 |
0.272 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268050 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19805059 |
GR directly regulates transcription of circadian clock components in mouse and human primary MSCs. Per2, E4bp4, Per1, and Timeless rapidly respond to glucocorticoid stimulation. Primary glucocorticoid receptor (GR) target genes are those at which GR occupies a nearby genomic glucocorticoid response element (GRE) and regulates target gene transcription |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Circadian clock |
| + |
NR3C1 | down-regulates quantity by repression
transcriptional regulation
|
NR4A3 |
0.294 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-132309 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15591535 |
We now show that the other nur factors, nurr1 and nor-1, are also subject to antagonism by gr and that this transrepression appears to involve direct protein-protein interactions between the dbds of gr and nur factors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR3C1 | up-regulates quantity by expression
transcriptional regulation
|
HNF4A |
0.376 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251684 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17978169 |
Electrophoretic mobility shift, chromatin immunoprecipitation (ChIP), and streptavidin DNA binding assays revealed that DEX increased binding of HNF4alpha to the HNF4-RE and that an interaction of GR and HNF4alpha occurred at this site. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
3.0
NR3C1
- 
- 