ArticleMolecular and cellular biology2003
Caspase 3-mediated inactivation of rac GTPases promotes drug-induced apoptosis in human lymphoma cells.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 46 citations in OpenAlex.
- The role of the enteric nervous system in the pathogenesis of Clostridioides difficile infection.Nature reviews. Gastroenterology & hepatology · 2025Review
- CD8Science advances · 2025Article
- Apoptosis and eryptosis: similarities and differences.Apoptosis : an international journal on programmed cell death · 2024Review
- p21-activated kinase 1 (PAK1) as a therapeutic target for cardiotoxicity.Archives of toxicology · 2022Review
- Platinum prodrug nanoparticles inhibiting tumor recurrence and metastasis by concurrent chemoradiotherapy.Journal of nanobiotechnology · 2022Article
- Cholinergic anti-inflammatory pathway ameliorates murine experimental Th2-type colitis by suppressing the migration of plasmacytoid dendritic cells.Scientific reports · 2022Article
- Deep phylogeny of cancer drivers and compensatory mutations.Communications biology · 2020Article
- The Small GTPase Rac1 Contributes to Extinction of Aversive Memories of Drug Withdrawal by Facilitating GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- RhoGDI deficiency induces constitutive activation of Rho GTPases and COX-2 pathways in association with breast cancer progression.Oncotarget · 2015Article
- ALDH1A1 mediates resistance of diffuse large B cell lymphoma to the CHOP regimen.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Activation of Rac1 GTPase promotes leukemia cell chemotherapy resistance, quiescence and niche interaction.Molecular oncology · 2013Article
- Activation of caspase-1 by the NLRP3 inflammasome regulates the NADPH oxidase NOX2 to control phagosome function.Nature immunology · 2013Article
- Regulation of the actin cytoskeleton in dendritic spines.Advances in experimental medicine and biology · 2012Review
- The rho GTPase Rac1 is required for proliferation and survival of progenitors in the developing forebrain.Developmental neurobiology · 2010Article
- Silencing of D4-GDI inhibits growth and invasive behavior in MDA-MB-231 cells by activation of Rac-dependent p38 and JNK signaling.The Journal of biological chemistry · 2009Article
- Physiological functions of caspases beyond cell death.The American journal of pathology · 2006Review
- Posttranslational myristoylation of caspase-activated p21-activated protein kinase 2 (PAK2) potentiates late apoptotic events.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Inhibition of Rac GTPase triggers a c-Jun- and Bim-dependent mitochondrial apoptotic cascade in cerebellar granule neurons.Journal of neurochemistry · 2005Article
- Rac1 inhibits apoptosis in human lymphoma cells by stimulating Bad phosphorylation on Ser-75.Molecular and cellular biology · 2004Article
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
The Rac members of the Rho family GTPases control signaling pathways that regulate diverse cellular activities, including cytoskeletal organization, gene transcription, and cell transformation. Rac is implicated in apoptosis, but little is known about the mechanism by which it responds to apoptotic stimuli. Here we demonstrate that endogenous Rac GTPases are caspase 3 substrates that are cleaved in human lymphoma cells during drug-induced apoptosis. Cleavage of Rac1 occurs at two unconventional caspase 3 sites, VVGD11/G and VMVD47/G, and results in inactivation of the GTPase and effector functions of the protein (binding to the p21-activated protein kinase PAK1). Expression of caspase 3-resistant Rac1 mutants in the cells suppresses drug-induced apoptosis. Thus, proteolytic inactivation of Rac GTPases represents a novel, irreversible mechanism of Rac downregulation that allows maximal cell death following drug treatment.
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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.