| + |
CAMK2G | down-regulates 
phosphorylation
|
NCOR2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-191777 |
Ser2407 |
AKVSGRPsSRKAKSP |
Homo sapiens |
|
| pmid |
sentence |
| 22888005 |
The kinase activity of camkii was essential for the activation of notch signaling. We also determined that camkii could enhance the association between notch1-ic and rbp-jk. Furthermore, the physical association between rbp-jk and smrt was substantially suppressed by camkii. We demonstrated that camkii directly bound and phosphorylated smrt at ser-1407, thereby facilitating smrt translocation from the nucleus to the cytoplasm and proteasome-dependent degradation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHUK | down-regulates
phosphorylation
|
NCOR2 |
0.414 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-129956 |
Ser2407 |
AKVSGRPsSRKAKSP |
Homo sapiens |
|
| pmid |
sentence |
| 15494311 |
Nf-kappab transcription requires ikkalpha to phosphorylate smrt on chromatin, stimulating the exchange of corepressor for coactivator complexes. Ikk directly phosphorylates smrt to stimulate nuclear export. Ikkalpha orchestrates smrt derepression, a prerequisite for nf-kappab transcription and survival. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IKK-complex | down-regulates
phosphorylation
|
NCOR2 |
0.407 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216393 |
Ser2407 |
AKVSGRPsSRKAKSP |
Homo sapiens |
|
| pmid |
sentence |
| 15494311 |
Nf-kappab transcription requires ikkalpha to phosphorylate smrt on chromatin, stimulating the exchange of corepressor for coactivator complexes. Ikk directly phosphorylates smrt to stimulate nuclear export. Ikkalpha orchestrates smrt derepression, a prerequisite for nf-kappab transcription and survival. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CAMK2A | down-regulates
phosphorylation
|
NCOR2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-191773 |
Ser2426 |
ASGDRPPsVSSVHSE |
Homo sapiens |
|
| pmid |
sentence |
| 22888005 |
We demonstrated that camkii directly bound and phosphorylated smrt at ser-1407, thereby facilitating smrt translocation from the nucleus to the cytoplasm and proteasome-dependent degradation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NR0B1 | up-regulates activity 
binding
|
NCOR2 |
0.392 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271785 |
|
|
Homo sapiens |
NCI-H295R Cell |
| pmid |
sentence |
| 19237537 |
The in vivo existence of an SF-1 corepressor complex consisting of DAX-1, RNF31, and SMRT at the steroidogenic promoters of the human StAR and CYP19 genes. We demonstrate that RNF31 is necessary for the stable association of the DAX-1 corepressor complex with chromatin-bound SF-1, thereby inhibiting the recruitment of coactivators and Pol II and controlling basal transcription levels of SF-1 target genes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SIRT1 | up-regulates
|
NCOR2 |
0.493 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253506 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22395773 |
In differentiated adipocyte cell lines, SIRT1 inhibits adipogenesis and enhances fat mobilization through lipolysis by suppressing the activity of PPARγ. SIRT1 achieves this by promoting the assembly of a corepressor complex, involving NCoR1 and SMRT, on the promoters of PPARγ target genes to repress their transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
NCOR2 | up-regulates
binding
|
SPEN |
0.467 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-107260 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11331609 |
Sharp is a potent transcriptional repressor whose repression domain (rd) interacts directly with smrt |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CDK2 | down-regulates activity
phosphorylation
|
NCOR2 |
0.43 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278306 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18838553 |
Cdk2 and Pin1 negatively regulate the transcriptional corepressor SMRT.|Cdk2 phosphorylates SMRT at consensus Cdk motifs to generate Pin1 binding sites and consequently targets SMRT for degradation, the latter also requiring the PPIase activity of Pin1 (XREF_FIG). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NCOR2 | down-regulates
acetylation
|
AR |
0.561 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-101286 |
|
|
Homo sapiens |
Breast Cancer Cell, Prostate Gland Cancer Cell |
| pmid |
sentence |
| 12771131 |
In this study we assessed the effect of smrt and dax-1 on ar and pr activity in the presence of both agonists and partial antagonists. We show that smrt and dax-1 repress agonist-dependent activity of both receptors, and the mechanism of repression includes disruption of the receptor dimer interactions rather than recruitment of histone deacetylases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FLT3 | down-regulates activity 
relocalization
|
NCOR2 |
0.258 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261538 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 14982881 |
We report here that the Flt3-ITD interferes with the transcriptional and biologic action of the PLZF transcriptional repressor. In the presence of Flt3-ITD, PLZF-SMRT interaction was reduced, transcriptional repression by PLZF was inhibited, and PLZF-mediated growth suppression of leukemia cells was partially blocked. Furthermore, overexpression of Flt3-ITD led to a partial relocalization of SMRT protein from the nucleus to the cytoplasm. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
NCOR2 | down-regulates
acetylation
|
PGR |
0.585 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-101289 |
|
|
Homo sapiens |
Breast Cancer Cell, Prostate Gland Cancer Cell |
| pmid |
sentence |
| 12771131 |
In this study we assessed the effect of smrt and dax-1 on ar and pr activity in the presence of both agonists and partial antagonists. We show that smrt and dax-1 repress agonist-dependent activity of both receptors, and the mechanism of repression includes disruption of the receptor dimer interactions rather than recruitment of histone deacetylases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NCOR2 | down-regulates quantity by repression
transcriptional regulation
|
PPARG |
0.746 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253508 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22395773 |
In differentiated adipocyte cell lines, SIRT1 inhibits adipogenesis and enhances fat mobilization through lipolysis by suppressing the activity of PPARγ. SIRT1 achieves this by promoting the assembly of a corepressor complex, involving NCoR1 and SMRT, on the promoters of PPARγ target genes to repress their transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NCOR2 | up-regulates
binding
|
BHLHE41 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-104489 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12897056 |
The spen protein, sharp (smrt/hdac1-associated repressor protein), was identified as a component of transcriptional repression complexes in both nuclear receptor and notch/rbp-jkappa signaling pathways. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SNW1 | down-regulates
binding
|
NCOR2 |
0.593 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-75785 |
|
|
Homo sapiens |
Myoblast |
| pmid |
sentence |
| 10713164 |
We present evidence that skip interacts with the cbf1 corepressor complex and that skip has a role in orchestrating the conversion of cbf1 from an smrt-hdac-tethered transcriptional repressor to a notchic-tethered activation complex. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Muscle |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
NCOR2 | up-regulates
binding
|
SNW1 |
0.593 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-74227 |
|
|
Homo sapiens |
Myoblast |
| pmid |
sentence |
| 10713164 |
Protein-protein interaction assays demonstrated interaction between skip and the corepressor smrt. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Muscle |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
RELA | down-regulates activity
relocalization
|
NCOR2 |
0.403 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261539 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 14982881 |
Furthermore, overexpression of Flt3-ITD led to a partial relocalization of SMRT protein from the nucleus to the cytoplasm. This indicates that shuttling of p65 was necessary for Flt3-ITD-mediated SMRT nuclear export. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
NCOR2 | up-regulates activity
binding
|
BCL6 |
0.629 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252240 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10898795 |
The POZ domains of BCL-6 and several other POZ proteins interact with corepressors N-CoR and SMRT. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
4.0
NCOR2
- 
- 