Id: | acc4901 |
Group: | 2sens |
Protein: | STAT3 |
Gene Symbol: | Stat3 |
Protein Id: | P42227 |
Protein Name: | STAT3_MOUSE |
PTM: | phosphorylation |
Site: | unclear |
Site Sequence: | |
Disease Category: | Immune system diseases |
Disease: | Psoriasis |
Disease Subtype: | |
Disease Cellline: | |
Disease Info: | |
Drug: | A-770041 |
Drug Info: | "A-770041 is a selective and orally active Src-family?Lck?inhibitor. A-770041 inhibits?Lck?with an?IC50?value of 147 nM with the presence of 1 mM ATP. A-770041 shows 300-fold selective to?Lck?over?Fyn, the?other?Src family kinase involved in T-cell signaling. A-770041 can be used for the research of acute rejection." |
Effect: | modulate |
Effect Info: | "Inhibiting the Lck signaling pathway (A-770041) can reduce the phosphorylation level of STAT3 in CD4? T cells, thereby weakening the Th1/Th17 inflammatory response, enhancing Treg expression, and improving the clinical features of psoriatic-like skin inflammation." |
Note: | |
Score: | 4.0 |
Pubmed(PMID): | 35576719 |
Sentence Index: | 35576719_6-7 |
Sentence: | "Results from the present study exhibit that p-Lck expression is enhanced in CD4+ T cells of IMQ-treated mice which is concomitant with enhanced clinical features of psoriatic inflammation (ear/back skin thickness, MPO activity, acanthosis/leukocytic infiltration) and molecular parameters (enhanced expression of p-Lck, p-PLCgamma, p-p38-MAPK, NFATc1, p-NFkB, TNF-alpha, IFN-gamma, p-STAT3, and IL-17A in CD4+ T cells). Inhibition of Lck signaling led to amelioration of clinical features of psoriasis through attenuation of Th1/Th17 immune responses and upregulation of Treg cells in IMQ-treated mice." |
Sequence & Structure:
MAQWNQLQQLDTRYLEQLHQLYSDSFPMELRQFLAPWIESQDWAYAASKESHATLVFHNLLGEIDQQYSRFLQESNVLYQHNLRRIKQFLQSRYLEKPMEIARIVARCLWEESRLLQTAATAAQQGGQANHPTAAVVTEKQQMLEQHLQDVRKRVQDLEQKMKVVENLQDDFDFNYKTLKSQGDMQDLNGNNQSVTRQKMQQLEQMLTALDQMRRSIVSELAGLLSAMEYVQKTLTDEELADWKRRQQIACIGGPPNICLDRLENWITSLAESQLQTRQQIKKLEELQQKVSYKGDPIVQHRPMLEERIVELFRNLMKSAFVVERQPCMPMHPDRPLVIKTGVQFTTKVRLLVKFPELNYQLKIKVCIDKDSGDVAALRGSRKFNILGTNTKVMNMEESNNGSLSAEFKHLTLREQRCGNGGRANCDASLIVTEELHLITFETEVYHQGLKIDLETHSLPVVVISNICQMPNAWASILWYNMLTNNPKNVNFFTKPPIGTWDQVAEVLSWQFSSTTKRGLSIEQLTTLAEKLLGPGVNYSGCQITWAKFCKENMAGKGFSFWVWLDNIIDLVKKYILALWNEGYIMGFISKERERAILSTKPPGTFLLRFSESSKEGGVTFTWVEKDISGKTQIQSVEPYTKQQLNNMSFAEIIMGYKIMDATNILVSPLVYLYPDIPKEEAFGKYCRPESQEHPEADPGSAAPYLKTKFICVTPTTCSNTIDLPMSPRTLDSLMQFGNNGEGAEPSAGGQFESLTFDMDLTSECATSPM
Select PDB:
No data.
Protein Tractability:
source: Open TargetsNo data.
PTM Intensity:
source: CPTACNo data.
PTM-Disease Association:
source: PTMDResidue | Position | State | Disease | Class | PMID |
---|---|---|---|---|---|
- | - | U | T-cell lymphoma | Phosphorylation | 9548458 |
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.