| + |
MAPK1 | up-regulates 
phosphorylation
|
STAT5A |
0.759 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-66239 |
Ser780 |
DSLDSRLsPPAGLFT |
Homo sapiens |
|
| pmid |
sentence |
| 10194762 |
Gh treatment of chinese hamster ovary cells stably transfected with the gh receptor (choa cells) led to rapid and transient activation of both stat5a and erk1 and erk2. these observations show, for the first time, direct physical interaction between erk and stat5a and also clearly identify serine 780 as a target for erk. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Ovary |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
MAPK3 | up-regulates
phosphorylation
|
STAT5A |
0.705 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-66247 |
Ser780 |
DSLDSRLsPPAGLFT |
Homo sapiens |
|
| pmid |
sentence |
| 10194762 |
Serine 780 is the only substrate in full-length stat5a for active erk |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Ovary |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
PTPN1 | down-regulates activity 
dephosphorylation
|
STAT5A |
0.674 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248428 |
Tyr694 |
LAKAVDGyVKPQIKQ |
Chlorocebus aethiops |
|
| pmid |
sentence |
| 10993888 |
A Cytosolic Protein-tyrosine Phosphatase PTP1B Specifically Dephosphorylates and Deactivates Prolactin-activated STAT5a and STAT5b |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
JAK2 | up-regulates
phosphorylation
|
STAT5A |
0.867 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-56827 |
Tyr694 |
LAKAVDGyVKPQIKQ |
Saccharomyces cerevisiae |
|
| pmid |
sentence |
| 9575217 |
Our mutational analysis suggests that the Stat5 SH2 domain is essential for the interaction with Jak2 and that the kinase domain of Jak2 is sufficient for Jak2-Stat5 interaction. Therefore, the Jak kinase domain may be all that is needed to cause Stat phosphorylation in situations where receptor docking is dispensable. [...] Most obviously, mutation of Tyr694 (Stat5a) or Tyr699 (Stat5b) to phenylalanine abolishes phosphorylation |
|
| Publications: |
1 |
Organism: |
Saccharomyces Cerevisiae |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, BCR-ABL in AML, FLT3 in AML, Onco-fusion proteins in AML, KIT in AML, Leptin Signaling |
| + |
SRC | up-regulates
phosphorylation
|
STAT5A |
0.75 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-111078 |
Tyr694 |
LAKAVDGyVKPQIKQ |
Homo sapiens |
|
| pmid |
sentence |
| 11641791 |
Src can thus directly tyrosine-phosphorylate the activation site of stat5 (tyr 694 in stat5a), and src may contribute to epo-induced signal transduction via stat5. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JAK3 | up-regulates
phosphorylation
|
STAT5A |
0.855 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-160672 |
Tyr694 |
LAKAVDGyVKPQIKQ |
Homo sapiens |
|
| pmid |
sentence |
| 18250158 |
For these assays, coexpression of wt jak3 with stat5a was found to result in tyrosine phosphorylation of stat5a (lane 2) mediated by jak3, since stat5a coexpressed with the kinase-inactive k855a mutant form of jak3 was not tyrosine phosphorylated. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-182817 |
Tyr694 |
LAKAVDGyVKPQIKQ |
Homo sapiens |
|
| pmid |
sentence |
| 19088846 |
For these assays, coexpression of wt jak3 with stat5a was found to result in tyrosine phosphorylation of stat5a (lane 2) mediated by jak3, since stat5a coexpressed with the kinase-inactive k855a mutant form of jak3 was not tyrosine phosphorylated. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
BTK | up-regulates activity
phosphorylation
|
STAT5A |
0.47 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250603 |
Tyr694 |
LAKAVDGyVKPQIKQ |
in vitro |
|
| pmid |
sentence |
| 11413148 |
Ectopically expressed BTK kinase domain was capable of tyrosine-phosphorylating STAT5A both in vitro and in vivo. BTK-mediated tyrosine phosphorylation of ectopically expressed wild type (but not Tyr(694) mutant) STAT5A enhanced its DNA binding activity. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | B-cell activation |
| + |
FLT3 | up-regulates activity
phosphorylation
|
STAT5A |
0.605 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-245069 |
Tyr694 |
LAKAVDGyVKPQIKQ |
Mus musculus |
32D Cell |
| pmid |
sentence |
| 17356133 |
in vitro kinase assays revealed that STAT5 is a direct target of Flt3 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261516 |
|
|
Mus musculus |
BA/F3 Cell |
| pmid |
sentence |
| 12796379 |
FLT3-ITDs induced a strong activation of STAT5. FLT3-ITD mutants induce an autophosphorylation of the receptor, interleukin 3-independent growth in Ba/F3 cells, and a strong STAT5 and mitogen-activated protein kinase (MAPK) activation. |
|
| Publications: |
2 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, FLT3 in AML, miRNA in AML, AML_TRIPLETS, FLT3-ITD in AML, FLT3-ITD signaling, Triple mutant AML |
| + |
PTPRG | up-regulates activity
dephosphorylation
|
STAT5A |
0.266 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254730 |
Tyr694 |
LAKAVDGyVKPQIKQ |
in vitro |
|
| pmid |
sentence |
| 25624455 |
PTPRG activation by the P1-WD peptide affected the tyrosine phosphorylation of several signaling molecules. Data analysis identified 31 molecules whose phosphorylation was modified in a statistically significant manner (Table I). inhibition of ABL1, BMX, BTK, DAB1, ITGB1, JAK2, KDR, KIT, LIMK1, MET, PDGFRB, SHC1, and VCL correlates with tyrosine dephosphorylation. In contrast, SRC inhibition correlates with hyperphosphorylation of the inhibitory Tyr530 residue and with dephosphorylation of the activatory Tyr419. Moreover, CDK2 and CTTN inhibition correlates with a hyperphosphorylation of the inhibitory Tyr15 and Tyr470, respectively. In contrast, a subgroup of 13 proteins, including BLNK, DOK2, ERBB2, GRIN2B, INSR, PDGFRA, PRKCD, PXN, STAT1, STAT2, STAT3, STAT5A, and ZAP70, appears to be activated by PTPRG activity. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
STAT5A | up-regulates 
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255682 |
|
|
Homo sapiens |
Culture Condition:CD34+ Cell |
| pmid |
sentence |
| 15353555 |
Here we report that a persistent activation of STAT5A in human CD34+ cells results in enhanced self-renewal. STAT5A drives the expression of a number of proto-oncogenes and cytokines in human CD34+ cells, as well as a number of erythroid-specific genes, favoring erythroid over myeloid differentiation and providing a long-term proliferative advantage for erythroid progenitors. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256233 |
|
|
Homo sapiens |
Mast Cell |
| pmid |
sentence |
| 20535135 |
Specifically, SCF-induced activation of JAK2 in human mast cells has been shown to activate STAT5 and STAT6. STAT5 contributes to mast cell homeostasis, by mediating proliferation, survival, and mediator release. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254302 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10072077 |
Here, we demonstrate that, while lymphoid development is normal, Stat5a/b mutant peripheral T cells are profoundly deficient in proliferation and fail to undergo cell cycle progression or to express genes controlling cell cycle progression |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, BCR-ABL in AML, FLT3 in AML, Onco-fusion proteins in AML, KIT in AML, miRNA in AML, AML_TRIPLETS, B-cell activation, FLT3-ITD in AML, FLT3-ITD signaling, Glucocorticoid receptor Signaling, Leptin Signaling, Triple mutant AML |
| + |
Gbeta | up-regulates
phosphorylation
|
STAT5A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270004 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10194762 |
Serine 780 is the only substrate in full-length stat5a for active erk |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Ovary |
| + |
pimozide | down-regulates activity
chemical inhibition
|
STAT5A |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260125 |
|
|
Homo sapiens |
Acute Myeloid Leukemia Cell |
| pmid |
sentence |
| 23264850 |
We have identified the psychotropic drug pimozide as an effective inhibitor of STAT5 function. Pimozide inhibits the tyrosine phosphorylation of STAT5, leading to the death of AML cells through the induction of apoptosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling |
| + |
STAT5A | up-regulates
|
FOXP3 |
0.486 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254365 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18270368 |
We demonstrate that the signal transducer and activator of transcription 5 (STAT5)-signaling cytokines, IL-2, IL-15 and to a lesser extent IL-7, induce FOXP3 up-regulation in vitro in activated human Teff cell |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254301 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18270368 |
We demonstrate that the signal transducer and activator of transcription 5 (STAT5)-signaling cytokines, IL-2, IL-15 and to a lesser extent IL-7, induce FOXP3 up-regulation in vitro in activated human Teff cell |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
NCOA1 | up-regulates
binding
|
STAT5A |
0.406 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-100258 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12954634 |
Ncoa-1/src-1 is an essential coactivator of stat5 that binds to the fdl motif in the alpha-helical region of the stat5 transactivation domain. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Breast |
| Pathways: | Acute Myeloid Leukemia, Glucocorticoid receptor Signaling |
| + |
NR3C1 | up-regulates
binding
|
STAT5A |
0.534 |
| 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 |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
BCL2L1 |
0.653 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261551 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 15626738 |
FLT3-ITD-TKD dual mutants induce hyperactivation of STAT5 and up-regulation of its downstream targets Bcl-x(L) and RAD51 in Ba/F3 cells |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, KIT in AML, FLT3-ITD in AML |
| + |
ERK1/2 | up-regulates
phosphorylation
|
STAT5A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270136 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10194762 |
Serine 780 is the only substrate in full-length stat5a for active erk |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Ovary |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, B-cell activation, FLT3-ITD in AML, FLT3-ITD signaling, Leptin Signaling, Triple mutant AML |
| + |
PTPN2 | down-regulates activity
dephosphorylation
|
STAT5A |
0.733 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-133547 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15780598 |
Upon ligand binding, IL-2R , IL-6R or LeptinR , IFN-_R , IFN-_R and PRLR or growth hormone (GH) receptor associated JAKs become activated. These JAKs mediate phosphorylation of specific tyrosine residues and recruit STATs. Activated STATs are released from the receptor and translocate to the nucleus. PTP1B dephosphorylates JAK2, TYK2 and STAT5 . The 45-kDa form of TC-PTP was shown to dephosphorylate JAK1 and JAK3 as well as STAT1, STAT3 and STAT5. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EGFR | up-regulates
binding
|
STAT5A |
0.821 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-146852 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16729043 |
We identified stat5 as a direct binding partner to egfr and erbb4 and discovered new recognition motifs for shc and stat5.Egf stimulation and subsequent phosphorylation of egfr at tyrosine y978, y998 and y869 would then subsequently lead to recruitment and activation of stat5. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-68159 |
|
|
Homo sapiens |
A-431 Cell |
| pmid |
sentence |
| 10358079 |
We identified stat5 as a direct binding partner to egfr and erbb4 and discovered new recognition motifs for shc and stat5.Egf stimulation and subsequent phosphorylation of egfr at tyrosine y978, y998 and y869 would then subsequently lead to recruitment and activation of stat5. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
PIM1 |
0.379 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261517 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 15498859 |
Pim-1 is a proto-oncogene and is known to be up-regulated by signal transducer and activator of transcription 5 (STAT5), which itself is a downstream target of FLT3 signaling. constitutively activated FLT3 signaling up-regulates Pim-1 expression in leukemia cells. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249606 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15498859 |
Pim-1 is know to be up regulated by signal transducer and activator of transcription 5 (stat5) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249621 |
|
|
|
|
| pmid |
sentence |
| 16146838 |
The results of 2 microarray experiments demonstrated that the aberrant activation of STAT proteins by Flt3-ITDs resulted in the up-regulation of several STAT5-responsive genes, such as Pim-1, Pim-2, and members of the SOCS (suppressor of cytokine signaling) protein family. These results are particularly interesting because recent data point to an important role of Pim kinases in the antiapoptosis of hematopoietic cells. |
|
| Publications: |
3 |
Organism: |
Mus Musculus, Homo Sapiens, |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD in AML, FLT3-ITD signaling |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
SOCS3 |
0.636 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261548 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 12468433 |
We have also found SOCS2 and SOCS3 specifically induced in 32D/Flt3-ITD, both of which are STAT3/5 target genes and known negative regulators of receptor signaling |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Leptin Signaling |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
PIM |
0.415 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255733 |
|
|
Homo sapiens |
MV4-11 Cell |
| pmid |
sentence |
| 29507660 |
FLT3-ITD is the most frequent tyrosine kinase mutation in acute myeloid leukemia (AML) associated with poor prognosis. We previously reported that activation of STAT5 confers resistance to PI3K/Akt inhibitors on the FLT3-ITD-positive AML cell line MV4-11 and 32D cells driven by FLT3-ITD (32D/ITD) but not by FLT3 mutated in the tyrosine kinase domain (32D/TKD). Here, we report the involvement of Pim kinases expressed through STAT5 activation in acquisition of this resistance. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD in AML |
| + |
CSF2RA | up-regulates
|
STAT5A |
0.591 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-32220 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 7716810 |
A major pathway which mediates the effects of gm-csf on macrophages involves activation of the latent transcription factor stat5a via a janus kinase 2 (jak2)-dependent pathway. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
CDKN1A |
0.326 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261518 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 15003515 |
Flt3 Mutation Activates p21WAF1/CIP1 Gene Expression Through the Action of STAT5. Co-transfection of p21 promoter-luciferase constructs with Flt3-ITD plasmid into K562 and BaF3 cells results in the induction of p21 promoter activity and a -692/-684 STAT site is important for the induction. STAT5a binds specifically to this element and Flt3-ITD enhances the protein binding to this site. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
HBB |
0.245 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251784 |
|
|
Mus musculus |
Hematopoietic Cell |
| pmid |
sentence |
| 9168989 |
We describe the roles of Stat5 and of these tyrosine residues in the EPOR in the erythroid differentiation of murine hematopoietic cell line SKT6 which produces hemoglobin in response to EPO. Chimeric receptors carrying the extracellular domain of the EGF receptor and the intracellular domain of the EPOR were introduced into SKT6 cells. Like EPO, EGF equally activated Stat5 and induced hemoglobin. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
STAT5A | up-regulates
|
Survival |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255578 |
|
|
Homo sapiens |
Monocyte |
| pmid |
sentence |
| 19436055 |
The alternative survival and proliferation pathway triggered by higher concentrations of GM-CSF is dependent on the dodecamer assembly and involves the Jak/STAT, Ras/mitogen-activated protein kinase, and PI-3 kinase pathways |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Skeletal Muscle |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
SOCS2 |
0.668 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261547 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 12468433 |
We have also found SOCS2 and SOCS3 specifically induced in 32D/Flt3-ITD, both of which are STAT3/5 target genes and known negative regulators of receptor signaling |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
STAT5A | down-regulates 
|
Cell_death |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256663 |
|
|
Homo sapiens |
Lymphoid Cell |
| pmid |
sentence |
| 14530308 |
Specific inhibition of Stat5a/b promotes apoptosis of IL-2-responsive primary and tumor-derived lymphoid cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAT5A | up-regulates quantity
transcriptional regulation
|
DNMT3A |
0.327 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255631 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26059451 |
… these data suggest that STAT5A positively regulates levels of DNMT3A, resulting in inactivation of tumor suppressor genes by epigenetic mechanisms in AML cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, miRNA in AML, AML_TRIPLETS, Triple mutant AML |
| + |
BCR-ABL | up-regulates activity
phosphorylation
|
STAT5A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255813 |
|
|
Mus musculus |
32D Cell |
| pmid |
sentence |
| 8642285 |
Phosphorylation of STAT1 and STAT5 was directly due to the tyrosine kinase activity of Bcr/Abl since it could be activated or deactivated by temperature shifting of cells expressing the Bcr/Abl ts mutant.These data suggest that STATs can be activated directly by Bcr/Abl, possibly bypassing JAK family kinase activation. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML, Onco-fusion proteins in AML |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
SLCO1B3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268990 |
|
|
|
|
| pmid |
sentence |
| 15840840 |
PRL enhanced the binding of Stat5a to the OATP1B3 promoter and DNA-protein binding was inhibited in competition assays by excess OATP1B3 and Stat5 consensus oligomers but not by mutant Stat5 oligomers.|PRL and GH induction of Oatp1b2 and OATP1B3 promoter activity required cotransfection of Stat5a and PRLRL or GHR. |
|
| Publications: |
1 |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
CISH |
0.669 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261544 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 15769897 |
The STAT5 target gene CIS, a member of the suppressor of cytokine signaling (SOCS) protein family, was highly induced by Flt3-ITD |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
RAD51 |
0.264 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261552 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 15626738 |
FLT3-ITD-TKD dual mutants induce hyperactivation of STAT5 and up-regulation of its downstream targets Bcl-x(L) and RAD51 in Ba/F3 cells |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling |
| + |
STAT5A | down-regulates
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256583 |
|
|
Homo sapiens |
Lymphoid Cell |
| pmid |
sentence |
| 14530308 |
Specific inhibition of Stat5a/b promotes apoptosis of IL-2-responsive primary and tumor-derived lymphoid cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, BCR-ABL in AML, FLT3 in AML, Onco-fusion proteins in AML, KIT in AML, miRNA in AML, AML_TRIPLETS, FLT3-ITD in AML, FLT3-ITD signaling, Triple mutant AML |
| + |
ponatinib | down-regulates activity
chemical inhibition
|
STAT5A |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259274 |
|
|
Homo sapiens |
Mast Cell |
| pmid |
sentence |
| 23539538 |
Ponatinib was found to inhibit the kinase activity of KIT G560V and KIT D816V in the human mast cell leukemia cell line HMC-1. In addition, ponatinib was found to block Lyn- and STAT5 activity in neoplastic mast cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAT5A | up-regulates
|
M1_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249510 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22025054 |
The activation of receptors for both GM-CSF and IFN-g stimulates the Jak kinaseSTAT transcription factor pathway, and an ISRE in the Irf5 promoter can bind STAT1 and STAT2, which suggests a possible mechanism for IRF5 expression induced by GM-CSF and IFN-g. Consequently, high expression of IRF5 results in polarization of the macrophage phenotype toward M1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
IRF5 |
0.289 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249508 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 25506346 |
The GM-CSF receptor forms a dodecamer structure and recruits JAK2, leading to the activation of STAT5, extracellular signal-regulated kinase (ERK), V-Akt murine thymoma viral oncogene homolog 1 (AKT), and the nuclear translocation of NF-kappaB and IRF5 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IL4R | up-regulates
|
STAT5A |
0.554 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254298 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20824124 |
Several cytokine receptors share subchains and targets. For example, the common gamma chain (CGC) is shared by IL2, IL4, IL7, IL9 and IL15 receptors that lead to the activation of STAT5 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAT5A | up-regulates
transcriptional regulation
|
Adipogenesis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-210146 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12540601 |
We have shown that stat5a is associated with the glucocorticoid receptor during adipogenesis in a highly regulated manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling, Leptin Signaling |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
PIM2 |
0.414 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249622 |
|
|
|
|
| pmid |
sentence |
| 16146838 |
The results of 2 microarray experiments demonstrated that the aberrant activation of STAT proteins by Flt3-ITDs resulted in the up-regulation of several STAT5-responsive genes, such as Pim-1, Pim-2, and members of the SOCS (suppressor of cytokine signaling) protein family. These results are particularly interesting because recent data point to an important role of Pim kinases in the antiapoptosis of hematopoietic cells. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261543 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 15769897 |
The serine-threonine kinase Pim-2 is a functionally relevant downstream target of STAT5. Here, we observed only a weak induction of Pim-2 by Flt3-D835Y compared to the effects of Flt3-ITD. |
|
| Publications: |
2 |
Organism: |
, Mus Musculus |
| + |
STAT5A | down-regulates quantity by repression
transcriptional regulation
|
MEF2C |
0.279 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254207 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21261500 |
STAT5 binds directly to the promoter region and potently mediates repression of MEF2C, probably via HDAC recruitment. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
PIM |
0.415 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259436 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15498859 |
Pim-1 is know to be up regulated by signal transducer and activator of transcription 5 (stat5) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD in AML |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
HBA1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251787 |
|
|
Mus musculus |
Hematopoietic Cell |
| pmid |
sentence |
| 9168989 |
We describe the roles of Stat5 and of these tyrosine residues in the EPOR in the erythroid differentiation of murine hematopoietic cell line SKT6 which produces hemoglobin in response to EPO. Chimeric receptors carrying the extracellular domain of the EGF receptor and the intracellular domain of the EPOR were introduced into SKT6 cells. Like EPO, EGF equally activated Stat5 and induced hemoglobin. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
IL3RA | up-regulates
|
STAT5A |
0.572 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-134862 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15795318 |
We previously demonstrated that integrin-dependent adhesion activates stat5a, a well known target of il-3-mediated signaling |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAT5A | up-regulates
|
Erythrocyte_differentiation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256074 |
|
|
Homo sapiens |
Culture Condition:CD34+ Cell |
| pmid |
sentence |
| 15353555 |
Here we report that a persistent activation of STAT5A in human CD34+ cells results in enhanced self-renewal. STAT5A drives the expression of a number of proto-oncogenes and cytokines in human CD34+ cells, as well as a number of erythroid-specific genes, favoring erythroid over myeloid differentiation and providing a long-term proliferative advantage for erythroid progenitors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
IGF1 |
0.437 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251743 |
|
|
Homo sapiens |
HEP-3B Cell |
| pmid |
sentence |
| 10050749 |
Growth hormone induces insulin-like growth factor-I gene transcription by a synergistic action of STAT5 and HNF-1α |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
miR-155 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255885 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23132946 |
We then showed that ectopic expression of MLL fusion genes in both human and mouse normal hematopoietic stem/progenitor cells could significantly down-regulate endogenous expression of miR-495 and that the depletion of MLL fusions resulted in the up-regulation of miR-495. Thus, our data suggest that there is an MLL-fusion–mediated negative regulation of the production of miR-495 in hematopoietic cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML |
| + |
STAP1 | up-regulates activity
binding
|
STAT5A |
0.416 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261821 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10679268 |
STAP-1 was tyrosine-phosphorylated by activated c-kit. An in vitro binding assay suggested that the STAP-1 SH2 domain interacted with several tyrosine-phosphorylated proteins including c-kit and STAT5. These suggest that STAP-1 functions as an adaptor molecule downstream of c-kit in hematopoietic stem cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAT5A | form complex 
binding
|
NR3C1/STAT5A |
0.534 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-44379 |
|
|
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 |
| + |
PTEN | down-regulates
dephosphorylation
|
STAT5A |
0.442 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-166481 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20596030 |
The forced expression of pten in the eol-1r cells dephosphorylated akt, erk and stat5 /eol-1r cells showed epigenetic silencing of the phosphatase and tensin homolog deleted on chromosome ten (pten) gene. Exposure of eol-1r cells to imatinib failed to dephosphorylate akt, erk and stat5, although pdgfr? Was effectively inactivated. The forced expression of pten negatively regulated these signal pathways and sensitized eol-1r cells to imatinib. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML, Onco-fusion proteins in AML, B-cell activation |
| + |
ERBB4 | up-regulates
binding
|
STAT5A |
0.81 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-146894 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16729043 |
We identified stat5 as a direct binding partner to egfr and erbb4 and discovered new recognition motifs for shc and stat5. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JAK2 | up-regulates activity
phosphorylation
|
STAT5A |
0.867 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249507 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 9575217 |
Jak2 kinase induces tyrosine phosphorylation, dimerization, nuclear translocation, and dna binding of a concomitantly expressed stat5 protein |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, BCR-ABL in AML, FLT3 in AML, Onco-fusion proteins in AML, KIT in AML, Leptin Signaling |
3.0
STAT5A
- 
- 