Caspase-3-mediated cleavage of ROCK I induces MLC phosphorylation and apoptotic membrane blebbing

By M. Sebbagh, C. Renvoizé, J. Hamelin, N. Riche, J. Bertoglio, J. Bréard. Nature Cell Biology, 2001

944 citations recorded by the source corpus.

Subfields: Cell Biology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b6c51b8737a9d983a8a13bd74a2817af2360f014

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Citations in the corpus

The nuts and bolts of AGC protein kinases (2010, background): “ROCK is also activated in apoptotic cells following cleavage of its auto-inhibitory C-terminus by caspase 3 (Ref”
Apoptotic cells induce migration of phagocytes via caspase-3-mediated release of a lipid attraction signal. (2003, background): “…that caspase-3-mediated activation of the Rho-associated Inhibition of iPLA2 but Not of cPLA2 in Apoptotic Cells Abrogates the Releasekinase ROCK I (Sebbagh et al., 2001) or of p21-activated kinase 2 (PAK2) (Rudel and Bokoch, 1997) are involved in of Chemotactic Activity LPC is generated upon…”
An Apoptotic 'Eat Me' Signal: Phosphatidylserine Exposure. (2015, background): “More than 500 substrates are cleaved by effector caspases [98], which are responsible for DNA fragmentation [99], membrane blebbing [100], nucleotide release [101], and PtdSer exposure.”
Germinal-center organization and cellular dynamics. (2007, background): “Studies in several cell types showed that early during apoptosis, caspases can cleave and activate the Rho kinase ROCK-I, in turn causing myosin light-chain kinase activation and inducing the events necessary for plasma-membrane blebbing (Coleman et al., 2001; Sebbagh et al., 2001; Shiratsuchi et al”
ROCKs: multifunctional kinases in cell behaviour (2003, background): “This occurs in vivo during apoptosis, when ROCK I is cleaved by CASPASE -3 to give rise to an active kinas”
Many cuts to ruin: a comprehensive update of caspase substrates (2003, background): “Apoptosis regulators Apaf-1 Apoptosome component Inactivated? SVTD (271) and a second unknown site 43, 44”
Biogenesis of extracellular vesicles (EV): exosomes, microvesicles, retrovirus-like vesicles, and apoptotic bodies (2013, neutral): “The available data suggest that membrane blebbing is, in part, mediated, by actin-myosin interaction [99, 100] (Fig.”
Classification, Functions, and Clinical Relevance of Extracellular Vesicles (2012, background): “Membrane blebbing requires phosphorylation of myosin light chain and Rho-associated coiled coil kinase I activity, which becomes constitutively active upon cleavage by caspase 3, induces a net increase in myosin light chain phosphorylation and subsequent membrane blebbing (Sebbagh et al., 2001).”
Gold nanorod assisted near-infrared plasmonic photothermal therapy (PPTT) of squamous cell carcinoma in mice. (2008, neutral): “Small increases in local temperature are known to result in disruption of nuclear and cytoskeletal assemblies and indeed, previous [44,84] and recent reports [29,72] indicate significant membrane blebbing [85–87] under hyperthermic conditions.”
Apoptosis: controlled demolition at the cellular level (2008, background): “Removal of the C-terminus of ROCK1 through caspase-mediated proteolysis results in constitutive activation of this kinase, leading to myosin light chain phosphorylation and contraction of actin bundle”
Structure of the Shroom-Rho Kinase Complex Reveals a Binding Interface with Monomeric Shroom That Regulates Cell Morphology and Stimulates Kinase Activity* (2016, background): “Additional mechanisms exist that affect Rock autoinhibitory interactions including lipid binding to the PH domain (29) and protease cleavage of the C terminus by caspase-3 (19) or granzyme B (18).”
Rho-Kinase/ROCK: A Key Regulator of the Cytoskeleton and Cell Polarity (2010, background): “Several lines of evidence suggest that the Rho-kinase signaling pathway also modulates cell survival and apoptosis, as Rho-kinase is known to be involved in morphological changes that occur during apoptosis [Coleman et al., 2001; Sebbagh et al., 2001; Sebbagh et al., 2005].”
Cell motility through plasma membrane blebbing (2008, background): “…these observations, PM blebbing was subsequently primarily viewed as a by-product of apoptotic and necrotic processes, during which cells display prominent blebs that are not related to cell locomotion ( Lewis, 1923 ; Torgerson and McNiven, 1998; Coleman et al., 2001 ; Sebbagh et al., 2001 ).”