Calpain and caspase: can you tell the difference?

By K. Wang. Trends in Neurosciences, 2000

965 citations recorded by the source corpus.

Subfields: Cell Biology, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/df3d7ae070012929c981ad01b07e0d02d81d52df

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Citations in the corpus

Cleavage Entropy as Quantitative Measure of Protease Specificity (2013, background): “In contrast to caspases, calpains cleave broader substrate spectra whilst showing overlap with caspases in some regions of substrate space [65].”
Pathophysiology of Cerebral Ischemia and Brain Trauma: Similarities and Differences (2004, background): “Because both caspase and calpain are activated in apoptotic neurons, the importance of these two neuronal death pathways and their interactions are an area of active investigation (Wang, 2000).”
PARP-1 cleavage fragments: signatures of cell-death proteases in neurodegeneration (2010, background): “Several cell substrates have been identified as calpain targets resulting in proteolytic breakdown to signature fragments of specific molecular weights [69,91,113].”
Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, background): “They are present in the cytosol as inactive precursors that are activated by increased cytosolic Ca [149,150].”
Neuronal Cell Death. (2018, positive): “Activated calpain I can cleave Bax and Bid, causing release of cytochrome c and AIF from mitochondria (145, 708).”
Ageing and neuronal vulnerability (2006, background): “Proteases such as caspases and calpains trigger apoptosis by degrading various structural protein”
Necrotic death as a cell fate. (2006, background): “While inhibition of PARP may lead to tumor development by promoting genomic instability (de Murcia et al. 1997; Wang et al. 1997) or may contribute to cell death as an anti-tumor strategy in cells lacking other components of DNA repair (de Murcia et al. 1997; Bryant et al. 2005; Farmer et al.…”
Caspase family proteases and apoptosis. (2005, background): “ribosyltransferase/PARP [ 38 ]. In apoptosis induced by ER stress, calpain’s functions are particularly salient because of the perturbed Ca2+ homeostasis.”