Source:http://linkedlifedata.com/resource/entrezgene/interaction/891-155807
Predicate | Object |
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rdf:type | |
entrezgene:pubmed |
pubmed-article:10958988,
pubmed-article:11531413,
pubmed-article:11691994,
pubmed-article:11878934,
pubmed-article:15265780,
pubmed-article:17586317,
pubmed-article:18445273,
pubmed-article:19275580,
pubmed-article:19275586,
pubmed-article:19344781,
pubmed-article:19458171,
pubmed-article:21489275,
pubmed-article:22552851,
pubmed-article:7474080,
pubmed-article:7474100,
pubmed-article:7494303,
pubmed-article:7666531,
pubmed-article:9094673,
pubmed-article:9520381,
pubmed-article:9560267
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entrezgene:interactant | |
entrezgene:geneRifText |
Data suggests that HIV-1 Vpr transactivation of the HIV-LTR promoter occurs through the inhibition of p300-associated cdc2-cyclin B kinase complex activity which enhances transcriptional activation by Rel A and p300,
HIV-1 Vpr causes increased levels of CyclinB1, Plk1, and Cdk1 in a complex with the nuclear transport and spindle assembly protein, importin beta,
HIV-1 Vpr inactivates the cdc2-cyclin B kinase complex by inactivating cdc25C, the phosphatase that dephosphorylates and activates cdc2,
HIV-1 Vpr inactivates the cdc2-cyclin B kinase complex by inhibiting the dephosphorylation of cdc2 tyrosine 15, leading to arrest in the G2 phase of the cell cycle,
HIV-1 Vpr induces accumulation of the G2 cell cycle protein cyclin B1 and activation of caspase-3 and caspase-9 in multidrug-resistant human colorectal cancer cells,
Inactivation of the cdc2-cyclin B kinase complex and arrest in the G2 phase of the cell cycle has been mapped to the C-terminus of HIV-1 Vpr, including amino acids 73, 80 and 84-96,
Inactivation of the cdc2-cyclin B kinase complex by HIV-1 Vpr leads to the activation of Poly(A) polymerase,
Rupture of HIV-1 Vpr-induced nuclear envelope herniations produces transient loss of the subcellular compartmentalization of Wee1, Cdc25C, cyclin B1, and presumably other soluble cellular components, resulting in their release into the cytoplasm,
The human Vpr interacting protein (hVIP/MOV34) is a likely cellular cofactor for HIV-1 Vpr inactivation of the cdc2-cyclin B kinase complex and induction of cell cycle arrest,
Vpr-induced cell cycle G2/M arrest reveals a dramatic increase in the amount of Cdk1, Cdc25C, and CyclinB1 bound to 14-3-3 theta
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entrezgene:keyphrase |
inhibits,
interacts with,
induces release of,
inactivates,
induces accumulation of
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