| Id: | acc2586 |
| Group: | 2sens |
| Protein: | AMPK |
| Gene Symbol: | PRKAA1 |
| Protein Id: | Q13131 |
| Protein Name: | AAPK1_HUMAN |
| PTM: | phosphorylation |
| Site: | Thr183 |
| Site Sequence: | MMSDGEFLRTSCGSPNYAAPE |
| Disease Category: | Cancer |
| Disease: | Lung Cancer |
| Disease Subtype: | NSCLC |
| Disease Cellline: | A549 |
| Disease Info: | |
| Drug: | "cis,cis,trans-[Pt(NH3)2Cl2(BEZ)(OH)] (CB)" |
| Drug Info: | - |
| Effect: | conducive |
| Effect Info: | "The phosphorylation of AMPK inhibits downstream HMGB1, NF-κB, and VEGFA, which may contribute to the inhibition of tumor angiogenesis and metastasis." |
| Note: | |
| Score: | 5.0 |
| Pubmed(PMID): | 34388483 |
| Sentence Index: | 34388483_7-8 |
| Sentence: | "Further cellular data also provided evidence that phosphorylation of AMPK, as a metabolic sensor, could suppress the downstream HMGB1, NF-kappaB, and VEGFA, which may contribute to the inhibition of angiogenesis and metastasis. Our study suggests that the antitumor action of CB and CP mechanistically distinct from the conventional platinum drugs and that functionalizing platinum-based agents with lipid-modulating agents may represent a novel practical strategy for cancer treatment." |
Sequence & Structure:
MRRLSSWRKMATAEKQKHDGRVKIGHYILGDTLGVGTFGKVKVGKHELTGHKVAVKILNRQKIRSLDVVGKIRREIQNLKLFRHPHIIKLYQVISTPSDIFMVMEYVSGGELFDYICKNGRLDEKESRRLFQQILSGVDYCHRHMVVHRDLKPENVLLDAHMNAKIADFGLSNMMSDGEFLRTSCGSPNYAAPEVISGRLYAGPEVDIWSSGVILYALLCGTLPFDDDHVPTLFKKICDGIFYTPQYLNPSVISLLKHMLQVDPMKRATIKDIREHEWFKQDLPKYLFPEDPSYSSTMIDDEALKEVCEKFECSEEEVLSCLYNRNHQDPLAVAYHLIIDNRRIMNEAKDFYLATSPPDSFLDDHHLTRPHPERVPFLVAETPRARHTLDELNPQKSKHQGVRKAKWHLGIRSQSRPNDIMAEVCRAIKQLDYEWKVVNPYYLRVRRKNPVTSTYSKMSLQLYQVDSRTYLLDFRSIDDEITEAKSGTATPQRSGSVSNYRSCQRSDSDAEAQGKSSEVSLTSSVTSLDSSPVDLTPRPGSHTIEFFEMCANLIKILAQ
Select PDB:
| Target | Drug name | MOA | Phase | Status | Disease | Source |
|---|---|---|---|---|---|---|
| PRKAA1 | ACADESINE | AMP-activated protein kinase, AMPK activator | 3 | - | cardiovascular disease | ATC |
| PRKAA1 | ACADESINE | AMP-activated protein kinase, AMPK activator | 1 | Completed | chronic lymphocytic leukemia | ClinicalTrials |
Note: Only show clinically investigational or approved drugs with protein targets.
Protein Tractability:
source: Open TargetsPTM Intensity:
source: CPTAC| PRKAA1-Thr183 | |
|---|---|
| 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 |
|---|---|---|---|---|---|
| T | 183 | D | Colon cancer/carcinoma | Phosphorylation | 25679763 |
| T | 183 | U | Breast cancer | Phosphorylation | 30413706 |
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.
