Article
Licensed
Unlicensed
Requires Authentication
Autoregulatory control of the p53 response by Siah-1L-mediated HIPK2 degradation
-
Marco A. Calzado
Published/Copyright:
July 30, 2009
Abstract
The different activities of the tumor suppressor p53 are tightly regulated by various negative and positive feedback loops, which allow accurate control of its function. Here we show that the p53-inducible ubiquitin E3 ligase Siah-1L can bind to the p53 phosphorylating kinase HIPK2 and thus allows its ubiquitination and proteasomal elimination. Siah-1L also eliminates the HIPK family member HIPK3, indicating that its activity is not restricted to one member of the HIPK family. The stimulating effect of HIPK2 on p53-triggered transcription is counteracted by Siah-1L, thus showing the occurrence of another negative feedback loop controlling the p53 response.
Received: 2009-3-20
Accepted: 2009-5-25
Published Online: 2009-07-30
Published in Print: 2009-10-01
©2009 by Walter de Gruyter Berlin New York
You are currently not able to access this content.
You are currently not able to access this content.
Articles in the same Issue
- Guest Editorial
- Highlight: ‘Regenerative Hepatology’
- Highlight: Regenerative Hepatology
- The do's and don'ts of p53 isoforms
- Mechanisms of liver disease: cross-talk between the NF-κB and JNK pathways
- Immunologic hurdles of therapeutic stem cell transplantation
- Ancestral vascular tube formation and its adoption by tumors
- Cellular plasticity of the pancreas
- Hepatic and pancreatic stellate cells in focus
- Interplay between host cell and hepatitis C virus in regulating viral replication
- Epidermal growth factor receptor signaling in liver cell proliferation and apoptosis
- The chemokine scavenging receptor D6 limits acute toxic liver injury in vivo
- Hepatic differentiation of pluripotent stem cells
- Protein Structure and Function
- Effect of curcumin on amyloidogenic property of molten globule-like intermediate state of 2,5-diketo-d-gluconate reductase A
- Cell Biology and Signaling
- Specific induction of migration and invasion of pancreatic carcinoma cells by RhoC, which differs from RhoA in its localisation and activity
- Autoregulatory control of the p53 response by Siah-1L-mediated HIPK2 degradation
Keywords for this article
apoptosis;
cell cycle;
HIPK2;
p53;
polyubiquitination;
Siah-1L;
transcription
Articles in the same Issue
- Guest Editorial
- Highlight: ‘Regenerative Hepatology’
- Highlight: Regenerative Hepatology
- The do's and don'ts of p53 isoforms
- Mechanisms of liver disease: cross-talk between the NF-κB and JNK pathways
- Immunologic hurdles of therapeutic stem cell transplantation
- Ancestral vascular tube formation and its adoption by tumors
- Cellular plasticity of the pancreas
- Hepatic and pancreatic stellate cells in focus
- Interplay between host cell and hepatitis C virus in regulating viral replication
- Epidermal growth factor receptor signaling in liver cell proliferation and apoptosis
- The chemokine scavenging receptor D6 limits acute toxic liver injury in vivo
- Hepatic differentiation of pluripotent stem cells
- Protein Structure and Function
- Effect of curcumin on amyloidogenic property of molten globule-like intermediate state of 2,5-diketo-d-gluconate reductase A
- Cell Biology and Signaling
- Specific induction of migration and invasion of pancreatic carcinoma cells by RhoC, which differs from RhoA in its localisation and activity
- Autoregulatory control of the p53 response by Siah-1L-mediated HIPK2 degradation
