ArticleCell death and differentiation2011
Caspase-2 is required for DNA damage-induced expression of the CDK inhibitor p21(WAF1/CIP1).
Article in Cell death and differentiation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- The PIDDosome controls cardiomyocyte polyploidization during postnatal heart development.Cell death and differentiation · 2026Article
- Senescent fibroblasts modulate the radiation response of neighboring epithelial cells.Cell death discovery · 2025Article
- Chemoproteomics Identifies State-Dependent and Proteoform-Selective Caspase-2 Inhibitors.Journal of the American Chemical Society · 2024Article
- Caspase-2 Inhibitor Blocks Tau Truncation and Restores Excitatory Neurotransmission in Neurons Modeling FTDP-17 Tauopathy.ACS chemical neuroscience · 2022Article
- The p53-caspase-2 axis in the cell cycle and DNA damage response.Experimental & molecular medicine · 2021Review
- The Role of Caspase-2 in Regulating Cell Fate.Cells · 2020Review
- Caspase-2 Substrates: To Apoptosis, Cell Cycle Control, and Beyond.Frontiers in cell and developmental biology · 2020Review
- Review
- The DEAD-box RNA helicase DDX41 is a novel repressor of p21The Journal of biological chemistry · 2017Article
- Caspase-2 resides in the mitochondria and mediates apoptosis directly from the mitochondrial compartment.Cell death discovery · 2016Article
- The tumor-modulatory effects of Caspase-2 and Pidd1 do not require the scaffold protein Raidd.Cell death and differentiation · 2015Article
- Caspase-2: the reinvented enzyme.Oncogene · 2015Review
- Deregulation of the MiR-193b-KRAS Axis Contributes to Impaired Cell Growth in Pancreatic Cancer.PloS one · 2015Article
- Death of p53-defective cells triggered by forced mitotic entry in the presence of DNA damage is not uniquely dependent on Caspase-2 or the PIDDosome.Cell death & disease · 2013Article
- The p90 ribosomal S6 kinase (RSK) inhibitor BI-D1870 prevents gamma irradiation-induced apoptosis and mediates senescence via RSK- and p53-independent accumulation of p21WAF1/CIP1.Cell death & disease · 2013Article
- Article
- Modulation of apoptotic pathways by human papillomaviruses (HPV): mechanisms and implications for therapy.Viruses · 2012Review
- p63 the guardian of human reproduction.Cell cycle (Georgetown, Tex.) · 2012Review
- Review
- Caspase-2 deficiency promotes aberrant DNA-damage response and genetic instability.Cell death and differentiation · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although caspase-2 represents the most conserved caspase across species and was the second caspase identified, its precise function remains enigmatic. In several cell types we show that knockdown of caspase-2 specifically impaired DNA damage-induced p21 expression, whereas overexpression of a caspase-2 mutant increased p21 levels. Caspase-2 did not influence p21 mRNA transcription; moreover, various inhibitors targeting proteasomal or non-proteasomal proteases, including caspases, could not restore p21 protein levels following knockdown of caspase-2. As, however, silencing of caspase-2 impaired exogenous expression of p21 constructs containing 3'-UTR sequences, our results strongly indicate that caspase-2 regulates p21 expression at the translational level. Intriguingly, unlike depletion of caspase-2, which prevented p21 expression and thereby reverted the γ-IR-induced senescent phenotype of wild-type HCT116 colon carcinoma cells into apoptosis, knockdown of none of the caspase-2-interacting components RAIDD, RIP or DNA-PKcs was able to mimic these processes. Together, our data suggest that this novel role of caspase-2 as a translational regulator of p21 expression occurs not only independently of its enzymatic activity but also does not require known caspase-2-activating platforms.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.