VENTX stimulates p16-INK4A transcription

Stable Identifier
R-HSA-8853921
Type
Reaction [omitted]
Species
Homo sapiens
Compartment
nucleoplasm
ReviewStatus
5/5
Locations in the PathwayBrowser
Expand all
General
SVG | 
PNG
Low
Medium
High
 | PPTX  | SBGN
VENTX stimulates p16-INK4A transcription
Click the image above or here to open this reaction in the Pathway Browser
The layout of this reaction may differ from that in the pathway view due to the constraints in pathway layout
Binding of VENTX to the p16-INK4A-specific CDKN2A promoter stimulates p16-INK4A expression. p16-INK4A acts as an inhibitor of cyclin-dependent kinases CDK4 and CDK6 and prevents CDK4/6-mediated inactivation of the RB1 tumor suppressor. Up-regulation of p16-INK4A contributes to VENTX-mediated cell cycle arrest (Wu et al. 2011). VENTX-mediated cell cycle arrest is implicated as an important step in differentiation of human hematopoietic cells (Gao et al. 2012).
Literature References
PubMed ID Title Journal Year
21325273 VentX trans-activates p53 and p16ink4a to regulate cellular senescence

Hager, M, Freeman, MR, Xiao, S, Ke, W, Gao, H, Wu, X, Zhu, Z

J. Biol. Chem. 2011
Participants
Input
Output
Participates
as an event of
This event is regulated
Positively by
Regulator
VENTX:CDKN2A Gene [nucleoplasm] (Homo sapiens)
Authored
Orlic-Milacic, M  (2019-06-28)
Reviewed
Vegi, NM  (2019-10-18)
Created
Orlic-Milacic, M  (2016-01-26)
Cite Us!