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Caspase 4, apoptosis-related cysteine peptidase

caspase-4, caspase-11, CASP4
This gene encodes a protein that is a member of the cysteine-aspartic acid protease (caspase) family. Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. Caspases exist as inactive proenzymes composed of a prodomain and a large and small protease subunit. Activation of caspases requires proteolytic processing at conserved internal aspartic residues to generate a heterodimeric enzyme consisting of the large and small subunits. This caspase is able to cleave and activate its own precursor protein, as well as caspase 1 precursor. When overexpressed, this gene induces cell apoptosis. Alternative splicing results in transcript variants encoding distinct isoforms. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: PrP, caspase-3, V1a, CHOP, CAN
Papers using caspase-4 antibodies
Involvement of caspase-4 in endoplasmic reticulum stress-induced apoptosis and Aβ-induced cell death
Tohyama Masaya et al., In The Journal of Cell Biology, 1996
... We used the following antibodies: anti–caspase-4 mAb (4B9; MBL International Corporation), anti–caspase-4 pAb ...
Papers on caspase-4
The nematocysts venom of Chrysaora helvola Brandt leads to apoptosis-like cell death accompanied by uncoupling of oxidative phosphorylation.
Shu et al., China. In Toxicon, Feb 2016
Interestingly, activation of caspase-4 other than caspase-3, -8, -9 and -1 was observed.
Gossypol induces pyroptosis in mouse macrophages via a non-canonical inflammasome pathway.
He et al., Guangzhou, China. In Toxicol Appl Pharmacol, Feb 2016
In this study, we found that in mouse macrophages, gossypol induced cell death characterized by rapid membrane rupture and robust release of HMGB1 and pro-caspase-11 comparable to ATP treatment, suggesting an induction of pyroptotic cell death.
Caspase-12, but Not Caspase-11, Inhibits Obesity and Insulin Resistance.
Saleh et al., Montréal, Canada. In J Immunol, Feb 2016
In this study, we investigated a role for caspase-11 and caspase-12 in obesity and insulin resistance.
Pyroptosis: Caspase-11 Unlocks the Gates of Death.
Martinon et al., Lausanne, Switzerland. In Immunity, Dec 2015
In this issue of Immunity, Núñez and colleagues report that caspase-11 cleaves the transmembrane channel pannexin-1, causing an efflux of cellular ATP that promotes a P2X7 receptor-dependent pyroptosis.
Caspase-11 Requires the Pannexin-1 Channel and the Purinergic P2X7 Pore to Mediate Pyroptosis and Endotoxic Shock.
Núñez et al., Ann Arbor, United States. In Immunity, Dec 2015
Priming the caspase-11 pathway in vivo with LPS or Toll-like receptor-3 (TLR3) agonist resulted in high mortality in wild-type mice after secondary LPS challenge, but not in Casp11(-/-), Panx1(-/-), or P2x7(-/-) mice.
Diverse mechanisms for inflammasome sensing of cytosolic bacteria and bacterial virulence.
Shao et al., Beijing, China. In Curr Opin Microbiol, Dec 2015
Caspase-11 and caspase-4/5 directly recognize bacterial LPS and then become activated.
Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling.
Dixit et al., San Francisco, United States. In Nature, Nov 2015
Intracellular lipopolysaccharide from Gram-negative bacteria including Escherichia coli, Salmonella typhimurium, Shigella flexneri, and Burkholderia thailandensis activates mouse caspase-11, causing pyroptotic cell death, interleukin-1β processing, and lethal septic shock.
Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death.
Shao et al., Beijing, China. In Nature, Nov 2015
Caspase-1 is activated by ligands of various canonical inflammasomes, and caspase-4, -5 and -11 directly recognize bacterial lipopolysaccharide, both of which trigger pyroptosis.
Potassium efflux fires the canon: Potassium efflux as a common trigger for canonical and noncanonical NLRP3 pathways.
Brough et al., Manchester, United Kingdom. In Eur J Immunol, Oct 2015
Murine caspase-11 and its human orthologues, caspase-4 and caspase-5, activate an inflammatory response following cytoplasmic recognition of cell wall constituents from Gram-negative bacteria, such as LPS.
The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease.
Dixit et al., New Haven, United States. In Nat Med, Mar 2015
BHB did not inhibit caspase-1 activation in response to pathogens that activate the NLR family, CARD domain containing 4 (NLRC4) or absent in melanoma 2 (AIM2) inflammasome and did not affect non-canonical caspase-11, inflammasome activation.
Caspase-11 and caspase-1 differentially modulate actin polymerization via RhoA and Slingshot proteins to promote bacterial clearance.
Amer et al., Columbus, United States. In Sci Rep, 2014
Caspase-11, independently of the inflammasome, also promotes phagolysosomal fusion.
Innate Immune Response in Brain, NF-Kappa B Signaling and Cystatins.
Kopitar-Jerala, Ljubljana, Slovenia. In Front Mol Neurosci, 2014
Stefin B deficient mice have increased caspase-11 expression and secreted higher amounts of pro-inflammatory cytokines.
Dangerous Liaisons: Caspase-11 and Reactive Oxygen Species Crosstalk in Pathogen Elimination.
Yilmaz et al., Gainesville, United States. In Int J Mol Sci, 2014
Recently, the focus of murine caspase-11 and human orthologs caspase-4, -5 research has been on their novel function to induce noncanonical inflammasome activation in direct response to Gram-negative bacterial infection.
The Role of Stefin B in Neuro-inflammation.
Kopitar-Jerala, Ljubljana, Slovenia. In Front Cell Neurosci, 2014
In our recent work, we demonstrated that stefin B-deficient mice were significantly more sensitive to the lethal lipopolysaccharide (LPS)-induced sepsis, due to increased caspase-11 expression and secreted higher amounts of pro-inflammatory cytokines IL-1β and IL-18.
Inhibition of inflammasome activation by Coxiella burnetii type IV secretion system effector IcaA.
Zamboni et al., Ribeirão Preto, Brazil. In Nat Commun, 2014
By using co-infection experiments, we determine that the infection of macrophages with C. burnetii inhibits the caspase-11-mediated non-canonical activation of the NLRP3 inflammasome induced by subsequent infection with Escherichia coli or Legionella pneumophila.
Caspase-11 increases susceptibility to Salmonella infection in the absence of caspase-1.
Monack et al., Stanford, United States. In Nature, 2012
non-canonical caspase-11 activation contributes to macrophage death during S. typhimurium infection
A genome-wide RNA interference screen identifies caspase 4 as a factor required for tumor necrosis factor alpha signaling.
Boutros et al., Heidelberg, Germany. In Mol Cell Biol, 2012
These experiments identify caspase 4 as a novel regulator of TNF-alpha-induced NF-kappaB signaling that is required for the activation of I-kappaB kinase.
TRIF licenses caspase-11-dependent NLRP3 inflammasome activation by gram-negative bacteria.
Fitzgerald et al., Worcester, United States. In Cell, 2012
Caspase-11 activation via the TLR4-TRIF-IFNbeta pathway synergizes with the NLRP3 pathway to coordinate caspase-1-dependent IL-1beta and IL-18 secretion and also leads to caspase-1-independent cell death.
An inactivating caspase 11 passenger mutation originating from the 129 murine strain in mice targeted for c-IAP1.
Duckett et al., Ann Arbor, United States. In Biochem J, 2012
found that, despite extensive backcrossing into a C57BL/6 background, c-IAP1(-/-) animals are also deficient in caspase 11
Caspase-4 is required for activation of inflammasomes.
Beer et al., Zürich, Switzerland. In J Immunol, 2012
Caspase-4 expression is essential for efficient nucleotide-binding domain leucine-rich repeat containing, Pyrin domain containing-3 and for absent in melanoma 2 inflammasome-dependent proIL-1beta activation in macrophages
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