Id: | acc0854 |
Group: | 2sens |
Protein: | AKT |
Gene Symbol: | Akt1 |
Protein Id: | P31750 |
Protein Name: | AKT1_MOUSE |
PTM: | phosphorylation |
Site: | Ser473 |
Site Sequence: | ERRPHFPQFSYSASGTA---- |
Disease Category: | Cancer |
Disease: | Neuroblastoma |
Disease Subtype: | |
Disease Cellline: | TBJ |
Disease Info: | |
Drug: | bortezomib |
Drug Info: | "Bortezomib is a reversible and selective proteasome inhibitor targeting the 20S proteasome with a Ki of 0.6 nM, used for the treatment of multiple myeloma in patients who have received at least two prior therapies and demonstrated disease progression on the last therapy. " |
Effect: | modulate |
Effect Info: | "Bortezomib inhibits the phosphorylation of Akt, thereby rendering drug-resistant TBJ/Neuro-2a cells sensitive to IFN-gamma plus TNF-alpha. It also effectively enhances the apoptosis of mouse neuroblastoma tumor cells in vitro." |
Note: | |
Score: | 4.0 |
Pubmed(PMID): | 16670342 |
Sentence Index: | 16670342_4-5 |
Sentence: | "The present studies provide the first evidence that bortezomib, a newly approved inhibitor of proteasome function, inhibits phosphorylation of Akt, induces the translocation of proapoptotic Bid, and potently enhances the apoptosis of murine neuroblastoma tumor cells in vitro. Furthermore, in that inhibitors of the Akt pathway can sensitize otherwise resistant TBJ/Neuro-2a cells to apoptosis induced by IFN-gamma plus TNF-alpha, we hypothesized that bortezomib also could sensitize these cells to IFN-gamma plus TNF-alpha." |
Sequence & Structure:
MNDVAIVKEGWLHKRGEYIKTWRPRYFLLKNDGTFIGYKERPQDVDQRESPLNNFSVAQCQLMKTERPRPNTFIIRCLQWTTVIERTFHVETPEEREEWATAIQTVADGLKRQEEETMDFRSGSPSDNSGAEEMEVSLAKPKHRVTMNEFEYLKLLGKGTFGKVILVKEKATGRYYAMKILKKEVIVAKDEVAHTLTENRVLQNSRHPFLTALKYSFQTHDRLCFVMEYANGGELFFHLSRERVFSEDRARFYGAEIVSALDYLHSEKNVVYRDLKLENLMLDKDGHIKITDFGLCKEGIKDGATMKTFCGTPEYLAPEVLEDNDYGRAVDWWGLGVVMYEMMCGRLPFYNQDHEKLFELILMEEIRFPRTLGPEAKSLLSGLLKKDPTQRLGGGSEDAKEIMQHRFFANIVWQDVYEKKLSPPFKPQVTSETDTRYFDEEFTAQMITITPPDQDDSMECVDSERRPHFPQFSYSASGTA
No data.
No data.
Protein Tractability:
source: Open TargetsNo data.
PTM Intensity:
source: CPTACNo data.
PTM-Disease Association:
source: PTMDResidue | Position | State | Disease | Class | PMID |
---|---|---|---|---|---|
S | 473 | D | Alzheimer's disease | Phosphorylation | 35834993 ;  36843923 |
S | 473 | D | Colonic inflammation | Phosphorylation | 36735734 |
S | 473 | D | Diabetes mellitus | Phosphorylation | 17130464 ;  16777975 ;  15033922 ;  15033922 ;  16777975 ;  17130464 ;  35739993 |
S | 473 | D | Turner syndrome | Phosphorylation | 33910978 |
S | 473 | U | Cardiomyopathy | Phosphorylation | 35358489 |
S | 473 | U | Diabetes mellitus | Phosphorylation | 35358489 |
S | 473 | U | Endometrial cancer/carcinoma | Phosphorylation | 16585156 |
S | 473 | U | Melanoma | Phosphorylation | 26565903 |
S | 473 | U | Non-small cell lung cancer | Phosphorylation | 35961388 |
S | 473 | U | Hepatocellular carcinoma | Phosphorylation | 33500384 |
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.