ArticleThe EMBO journal1999
Inhibition of apoptosis and clonogenic survival of cells expressing crmA variants: optimal caspase substrates are not necessarily optimal inhibitors.
Article in The EMBO journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 88 citations in OpenAlex.
- Degradation of Host Proteins and Apoptosis Induced by Foot-and-Mouth Disease Virus 3C Protease.Pathogens (Basel, Switzerland) · 2021Article
- Serpin functions in host-pathogen interactions.PeerJ · 2018Article
- A bifunctional protein regulates mitochondrial protein synthesis.Nucleic acids research · 2014Article
- TRAIL treatment provokes mutations in surviving cells.Oncogene · 2010Article
- The enigma of caspase-2: the laymen's view.Cell death and differentiation · 2009Review
- Determination of cell survival by RING-mediated regulation of inhibitor of apoptosis (IAP) protein abundance.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Specificity and reactive loop length requirements for crmA inhibition of serine proteases.Protein science : a publication of the Protein Society · 2005Article
- The apoptotic pathway triggered by the Fhit protein in lung cancer cell lines is not affected by Bcl-2 or Bcl-x(L) overexpression.Oncogene · 2004Article
- Apaf-1 and caspase-9 accelerate apoptosis, but do not determine whether factor-deprived or drug-treated cells die.The Journal of cell biology · 2004Article
- Hsp70 mutant proteins modulate additional apoptotic pathways and improve cell survival.Cell stress & chaperones · 2004Article
- Neuroprotection and acute spinal cord injury: a reappraisal.NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics · 2004Review
- A decade of caspases.Oncogene · 2003Review
- CrmA gene expression protects mice against concanavalin-A-induced hepatitis by inhibiting IL-18 secretion and hepatocyte apoptosis.Gene therapy · 2003Article
- Subcellular localization of CrmA: identification of a novel leucine-rich nuclear export signal conserved in anti-apoptotic serpins.The Biochemical journal · 2003Article
- Baculovirus apoptotic suppressor P49 is a substrate inhibitor of initiator caspases resistant to P35 in vivo.The EMBO journal · 2002Article
- Tumour necrosis factor-induced activation of c-Jun N-terminal kinase is sensitive to caspase-dependent modulation while activation of mitogen-activated protein kinase (MAPK) or p38 MAPK is not.The Biochemical journal · 2002Article
- The anti-apoptotic activity of XIAP is retained upon mutation of both the caspase 3- and caspase 9-interacting sites.The Journal of cell biology · 2002Article
- Mitochondrial dysfunction is an essential step for killing of non-small cell lung carcinomas resistant to conventional treatment.Oncogene · 2002Article
- Direct inhibition of caspase 3 is dispensable for the anti-apoptotic activity of XIAP.The EMBO journal · 2001Article
- The Drosophila caspase DRONC is regulated by DIAP1.The EMBO journal · 2000Article
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
To study the role of various caspases during apoptosis, we have designed a series of caspase inhibitors based on the cowpox virus cytokine response modifier A (crmA) protein. Wild-type crmA inhibits caspases 1 and 8 and thereby protects cells from apoptosis triggered by ligation of CD95 or tumour necrosis factor (TNF) receptors, but it does not protect against death mediated by other caspases. By replacing the tetrapeptide pseudosubstrate region of crmA (LVAD) with tetrapeptides that are optimal substrates for the different families of caspases, or with the four residues from the cleavage site of the baculovirus protein p35 (DQMD), we have generated a family of caspase inhibitors that show altered ability to protect against cell death. Although DEVD is the optimal substrate for caspase 3, crmA DEVD was degraded rapidly and was a weaker inhibitor than crmA DQMD, which was not degraded. Unlike wild-type crmA and crmA DEVD, crmA DQMD was able to inhibit apoptosis caused by direct activation of caspase 3 and protected lymphoid cells from death induced by radiation and dexamethasone. Significantly, the protected cells were capable of sustained growth.
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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.