| Id: | acc3543 |
| Group: | 2sens |
| Protein: | JNK |
| Gene Symbol: | MAPK8 |
| Protein Id: | P45983 |
| Protein Name: | MK08_HUMAN |
| PTM: | phosphorylation |
| Site: | Tyr185 |
| Site Sequence: | AGTSFMMTPYVVTRYYRAPEV |
| Disease Category: | Cancer |
| Disease: | Glioma |
| Disease Subtype: | |
| Disease Cellline: | H4 |
| Disease Info: | |
| Drug: | gefitinib |
| Drug Info: | "Gefitinib is an oral, selective epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) used in the treatment of certain types of non - small cell lung cancer." |
| Effect: | modulate |
| Effect Info: | "Gefitinib induces glioma cell death by promoting the phosphorylation of IRE1, apoptosis signal-regulating kinase-1 (Ask1), and c-Jun N-terminal kinase (JNK)." |
| Note: | |
| Score: | 4.0 |
| Pubmed(PMID): | 33920356 |
| Sentence Index: | 33920356_7-8 |
| Sentence: | "Three branches of ER stress, namely Activating Transcription Factor-6 (ATF6), Protein Kinase R (PKR)-Like ER Kinase (PERK), and Inositol-Requiring Enzyme 1 (IRE1), were activated by gefitinib, along with the elevation of intracellular free Ca2+, Reactive Oxygen Species (ROS), and NADPH Oxidase2/4 (NOX2/4). Specifically, elevated IRE1 phosphorylation, Tumor Necrosis Factor (TNF) Receptor-Associated Factor-2 (TRAF2) expression, Apoptosis Signal-Regulating Kinase-1 (Ask1) phosphorylation, c-Jun N-Terminal Kinase (JNK) phosphorylation, and Noxa expression appeared in gefitinib-treated glioma cells." |
Sequence & Structure:
MSRSKRDNNFYSVEIGDSTFTVLKRYQNLKPIGSGAQGIVCAAYDAILERNVAIKKLSRPFQNQTHAKRAYRELVLMKCVNHKNIIGLLNVFTPQKSLEEFQDVYIVMELMDANLCQVIQMELDHERMSYLLYQMLCGIKHLHSAGIIHRDLKPSNIVVKSDCTLKILDFGLARTAGTSFMMTPYVVTRYYRAPEVILGMGYKENVDLWSVGCIMGEMVCHKILFPGRDYIDQWNKVIEQLGTPCPEFMKKLQPTVRTYVENRPKYAGYSFEKLFPDVLFPADSEHNKLKASQARDLLSKMLVIDASKRISVDEALQHPYINVWYDPSEAEAPPPKIPDKQLDEREHTIEEWKELIYKEVMDLEERTKNGVIRGQPSPLGAAVINGSQHPSSSSSVNDVSSMSTDPTLASDTDSSLEAAAGPLGCCR
Select PDB:
| Target | Drug name | MOA | Phase | Status | Disease | Source |
|---|---|---|---|---|---|---|
| MAPK8 | BENTAMAPIMOD | c-Jun N-terminal kinase, JNK inhibitor | 2 | Completed | endometriosis | ClinicalTrials |
| MAPK8 | TANZISERTIB | c-Jun N-terminal kinase 1 inhibitor | 2 | Terminated | idiopathic pulmonary fibrosis | ClinicalTrials |
| MAPK8 | TANZISERTIB | c-Jun N-terminal kinase 1 inhibitor | 2 | Terminated | lupus erythematosus | ClinicalTrials |
| MAPK8 | CC-401 | c-Jun N-terminal kinase 1 inhibitor | 1 | Terminated | myeloid leukemia | ClinicalTrials |
Note: Only show clinically investigational or approved drugs with protein targets.
Protein Tractability:
source: Open TargetsPTM Intensity:
source: CPTAC| MAPK8-Tyr185 | |
|---|---|
| Cancer | Intensity |
| BRCA | |
| COAD | -0.707 |
| HGSC | 0.707 |
| ccRCC | |
| GBM | |
| HNSC | |
| LUAD | |
| LUSC | |
| non_ccRCC | |
| PDAC | |
| UCEC | |
PTM-Disease Association:
source: PTMD| Residue | Position | State | Disease | Class | PMID |
|---|---|---|---|---|---|
| Y | 185 | U | Pancreatic cancer | Phosphorylation | 37016317 |
| Y | 185 | U | Type 2 diabetes | Phosphorylation | 21931634 |
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.
