Id: | acc0175 |
Group: | 2sens |
Protein: | STAT5 |
Gene Symbol: | STAT5A |
Protein Id: | P42229 |
Protein Name: | STA5A_HUMAN |
PTM: | phosphorylation |
Site: | Tyr694 |
Site Sequence: | PVLAKAVDGYVKPQIKQVVPE |
Disease Category: | Cancer |
Disease: | Leukemia |
Disease Subtype: | AML-M5 |
Disease Cellline: | MV4-11 |
Disease Info: | |
Drug: | cabozantinib |
Drug Info: | "Cabozantinib is a multi-targeted tyrosine kinase inhibitor that acts on MET, VEGFR1/2/3, RET, AXL, and other kinases, approved for the treatment of progressive metastatic medullary thyroid cancer, advanced renal cell carcinoma after prior anti-angiogenic therapy, and hepatocellular carcinoma following sorafenib failure. " |
Effect: | modulate |
Effect Info: | "Cabozantinib inhibits the phosphorylation of FLT3, STAT5, AKT, and ERK, thereby inhibiting and preventing the growth of MV4 - 11 tumor cells." |
Note: | |
Score: | 4.0 |
Pubmed(PMID): | 27060207 |
Sentence Index: | 27060207_3-4 |
Sentence: | "However, K562, OCI-AML3 and THP-1 (leukemia cell lines lacking FLT3-ITD) were resistant to cabozantinib, showing IC50 values in the micromolar range. Cabozantinib arrested MV4-11 cell growth at the G0/G1 phase within 24 h, which was associated with decreased phosphorylation of FLT3, STAT5, AKT and ERK." |
Sequence & Structure:
MAGWIQAQQLQGDALRQMQVLYGQHFPIEVRHYLAQWIESQPWDAIDLDNPQDRAQATQLLEGLVQELQKKAEHQVGEDGFLLKIKLGHYATQLQKTYDRCPLELVRCIRHILYNEQRLVREANNCSSPAGILVDAMSQKHLQINQTFEELRLVTQDTENELKKLQQTQEYFIIQYQESLRIQAQFAQLAQLSPQERLSRETALQQKQVSLEAWLQREAQTLQQYRVELAEKHQKTLQLLRKQQTIILDDELIQWKRRQQLAGNGGPPEGSLDVLQSWCEKLAEIIWQNRQQIRRAEHLCQQLPIPGPVEEMLAEVNATITDIISALVTSTFIIEKQPPQVLKTQTKFAATVRLLVGGKLNVHMNPPQVKATIISEQQAKSLLKNENTRNECSGEILNNCCVMEYHQATGTLSAHFRNMSLKRIKRADRRGAESVTEEKFTVLFESQFSVGSNELVFQVKTLSLPVVVIVHGSQDHNATATVLWDNAFAEPGRVPFAVPDKVLWPQLCEALNMKFKAEVQSNRGLTKENLVFLAQKLFNNSSSHLEDYSGLSVSWSQFNRENLPGWNYTFWQWFDGVMEVLKKHHKPHWNDGAILGFVNKQQAHDLLINKPDGTFLLRFSDSEIGGITIAWKFDSPERNLWNLKPFTTRDFSIRSLADRLGDLSYLIYVFPDRPKDEVFSKYYTPVLAKAVDGYVKPQIKQVVPEFVNASADAGGSSATYMDQAPSPAVCPQAPYNMYPQNPDHVLDQDGEFDLDETMDVARHVEELLRRPMDSLDSRLSPPAGLFTSARGSLS
Select PDB:
No data.
Protein Tractability:
source: Open TargetsPTM Intensity:
source: CPTACSTAT5A-Tyr694 | |
---|---|
Cancer | Intensity |
BRCA | -0.21 |
COAD | 0.081 |
HGSC | 2.396 |
ccRCC | 0.242 |
GBM | -0.214 |
HNSC | 0.119 |
LUAD | 0.595 |
LUSC | 0.038 |
non_ccRCC | -1.223 |
PDAC | -0.376 |
UCEC | -1.449 |
PTM-Disease Association:
source: PTMDResidue | Position | State | Disease | Class | PMID |
---|---|---|---|---|---|
Y | 694 | D | Head and neck squamous cell carcinoma | Phosphorylation | 21281788 |
Y | 694 | D | Sjogren's syndrome | Phosphorylation | 36072585 |
Y | 694 | N | Large granular lymphocytic leukemia | Phosphorylation | 23596048 |
Y | 694 | U | Glioblastoma | Phosphorylation | 22729867 |
Y | 694 | U | Colon cancer | Phosphorylation | 23733954 |
Y | 694 | U | Human immunodeficiency virus infectious disease | Phosphorylation | 21716071 |
State Note: Based on the distinct PTM states in diseases, PTMD classified all disease-associated PTMs into six classes, including whether the up-regulation (U) or down-regulation (D) of PTM levels, the absence (A) or presence (P) of PTMs, and the creation (C) or disruption (N) of PTM sites are associated with diseases.
PTM-Drug Perturbation Response:
source: DecryptMNo data.
Function score:
source: funscoRNo data.