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anti-Human Caspase 4 Antikörper:
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Human Monoclonal Caspase 4 Primary Antibody für ELISA, ICC - ABIN265762
Kenneth, Younger, Hughes, Marcotte, Barker, Saunders, Duckett: An inactivating caspase 11 passenger mutation originating from the 129 murine strain in mice targeted for c-IAP1. in The Biochemical journal 2012
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Mouse (Murine) Monoclonal Caspase 4 Primary Antibody für WB - ABIN2688867
Kayagaki, Warming, Lamkanfi, Vande Walle, Louie, Dong, Newton, Qu, Liu, Heldens, Zhang, Lee, Roose-Girma, Dixit: Non-canonical inflammasome activation targets caspase-11. in Nature 2011
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Human Polyclonal Caspase 4 Primary Antibody für IHC (fro), WB - ABIN550328
Kuida, Lippke, Ku, Harding, Livingston, Su, Flavell: Altered cytokine export and apoptosis in mice deficient in interleukin-1 beta converting enzyme. in Science (New York, N.Y.) 1995
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Human Polyclonal Caspase 4 Primary Antibody für IHC (fro), WB - ABIN550329
Gracie, Robertson, McInnes: Interleukin-18. in Journal of leukocyte biology 2003
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Mouse (Murine) Polyclonal Caspase 4 Primary Antibody für WB - ABIN4288033
Tomura, de Rivero Vaccari, Keane, Bramlett, Dietrich: Effects of therapeutic hypothermia on inflammasome signaling after traumatic brain injury. in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 2012
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Human Polyclonal Caspase 4 Primary Antibody für IHC (p), WB - ABIN3043186
Ji, Yan, Li, Lai, Liu: Therapeutic effects of intrathecal versus intravenous monosialoganglioside against bupivacaine-induced spinal neurotoxicity in rats. in Biomedicine & pharmacotherapy = Biome?decine & pharmacothe?rapie 2015
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Mouse (Murine) Polyclonal Caspase 4 Primary Antibody für WB - ABIN6677591
Zuo, Kong, Wang, Liu, Wang, Wan, Yan, Zhang, Tang, Zhang, Lyu, Li, Shan, Qian, Shen, Yu: CRTH2 promotes endoplasmic reticulum stress-induced cardiomyocyte apoptosis through m-calpain. in EMBO molecular medicine 2018
Human Polyclonal Caspase 4 Primary Antibody für ELISA, WB - ABIN268673
Munday, Vaillancourt, Ali, Casano, Miller, Molineaux, Yamin, Yu, Nicholson: Molecular cloning and pro-apoptotic activity of ICErelII and ICErelIII, members of the ICE/CED-3 family of cysteine proteases. in The Journal of biological chemistry 1995
Human Polyclonal Caspase 4 Primary Antibody für WB - ABIN222883
Kim, Zhang, Hitomi, Lee, Mukherjee: Endoplasmic reticulum stress-induced caspase-4 activation mediates apoptosis and neurodegeneration in INCL. in Human molecular genetics 2006
these findings reveal a novel role for caspase-4 as a sensor molecule to amplify pro-inflammatory responses when macrophage encounters Entamoeba histolytica
this study shows that caspase-4 induces activation of caspase-1 and secretion of IL-1beta in response to dengue virus serotype-2 infection, without the need for secondary signals to stimulate the assembly of the inflammasome
Results implicate pyroptosis induced by the CASP11/4-GSDMD pathway in the pathogenesis of alcoholic hepatitis
Results indicate functional differences between human caspase-4 and murine caspase-11.
The last four amino acids of the NleF carboxy terminus are essential in inhibiting caspase-4-dependent inflammatory cell death.
Pathophysiological studies showed that the overexpression of the CASP4 gene was involved in the loss of proximal tubules and renal injury in nephropathic cystinosis patients. Considering kidney's key roles in sodium filtration and reabsorption CASP4 genes are involved in Blood Pressure regulation.
We propose that microglial caspase-4 expression contributes to the cognitive impairments in Alzheimer's disease (AD), and that further study of caspase-4 will enhance our understanding of AD pathogenesis and may lead to novel therapeutic targets in AD.
this study shows that activation of caspase-4 is mediated by interactions with endotoxin-rich membrane interfaces rather than by endotoxin monomers
Specific activation of caspase-3 and caspase-4 was found in proplatelets. Consistent with previous observations of caspase-4 autoactivation in response to endoplasmic reticulum (ER) stress, several ER stress marker proteins were expressed during proplatelet formation.
apoptosis is induced by rhein traditional Chinese medicine via induction of endoplasmic reticulum stress, caspase-4 and intracellular calcium in primary human hepatic HL-7702 cells
Caspase-4 and caspase-5 mediate IL-1alpha and IL-1beta release from human monocytes after lipopolysaccharides stimulation.
both caspase-4 and caspase-5 are functionally important for appropriate responses to intracellular Gram-negative bacteria.
caspase-4 activation alone is sufficient to induce pyroptosis, this process depends on the NLRP3 inflammasome activation to drive IL-1beta maturation.
This study reveled that CASP4 having a central role in the bipolar disease and schizophrenia manifestation.
NF-kappaB can mediate Fas-induced apoptosis through caspase-4 protease
implicate caspase-4 as a critical regulator of noncanonical inflammasome activation that initiates defense against bacterial pathogens in primary macrophages
this study has identified epithelial-expressed caspases-4 and -5 as biomarkers with diagnostic and therapeutic potential in colorectal cancer.
Authors observed increases in the endoplasmic reticulum stress markers BiP and cleaved caspase-4 in Duchenne muscular dystrophy patient biopsies, compared with controls.
The caspase-4/11 inflammasome also governs activation of the proinflammatory cytokine, interleukin (IL)-18, in response to intracellular and extracellular enteric pathogens.
function of caspase-4/5/11 represents a new mode of pattern recognition in immunity and also an unprecedented means of caspase activation
caspase-1/11 pathway plays an important role in the induction of liver adaptive immunity against Trypanosoma cruzi acute infection
suggest caspase-11 specificity may be determined outside the known substrate motif and identifies substrates cleaved preferentially by caspase-1, providing new opportunities to uniquely target inflammatory caspases
Defective STAT1 activation in Casp11(-/-) colons during disease progression.
Caspase-11 promotes renal epithelial cell apoptosis by activating the caspase-3-dependent apoptotic pathway in cisplatin-induced acute kidney injury.
It has been shown that Scgb3a2 chaperones LPS to the cytosol through the cell surface receptor syndecan-1; this leads to pyroptotic lung cancer cell death driven by caspase-11.
Caspase-11 has to be present with caspase-8 to support tumor necrosis factor- and interferon-beta-dependent tissue injury first observed in the small intestine and later in spleen and thymus. Caspase-11 enhanced the activation of caspase-8 and extrinsic cell death within the lower small intestine. Combined pyroptotic and apoptotic signaling mediated endotoxemia independently of cytokines involved cell death pathways.
Together, our findings demonstrate that TRIF signaling is required for caspase-11-dependent immune responses and lethality in endotoxemia and sepsis, and provide novel mechanistic insights into how LPS induces caspase-11 activation during bacterial infection.
comparing the activities of caspase-1 and -11 in HyCoSuL screens and with three endogenous protein substrates, they conclude that caspase-11 has highly restricted substrate specificity, preferring gasdermin D over all other substrates examined.
The enzymatic activities of caspase-1 and caspase-11 are required for growth inhibition in different cell types.These results reveal that these proteases have important functions beyond the direct induction of pyroptosis and proinflammatory cytokine secretion in the control of growth and elimination of cytosolic bacteria.
Together, these data suggest that caspase-11/IL-1alpha pathway plays an important role in defending against Klebsiella pneumoniae by recruiting neutrophils in the early stage of infection.
Results indicate functional differences between human caspase-4 and murine caspase-11 (caspase 4).
The results demonstrate the activation of the caspase 1 precursor by caspase 11 and suggest a new mechanism of protection of Theiler murine encephalomyelitis virus-infected astrocytes from apoptosis.
Data suggest that Brucella melitensis effector protein TcpB suppresses caspase-4/11--mediated inflammation, subverting inflammasome activation in mouse macrophages; TcpB induces ubiquitination/degradation of caspase-4/11; TcpB suppresses caspase-4/11--mediated pyroptosis and proinflammatory responses induced by lipopolysaccharide.
systemic exposure to the bacterial endotoxin lipopolysaccharide (LPS) causes severe endothelial pyroptosis that is mediated by the inflammatory caspases, human caspases 4/5 in human ECs, or the murine homolog caspase-11 in mice in vivo.
Caspase-l, Caspase-11 and Dectin-1/syk pathway are involved in the IL-1beta generation in fungal keratosis.
These data indicate that the caspase-11-mediated innate immune response plays a crucial role in defending against Acinetobacter baumannii.
Caspase-11 targets cofilin via the RhoA GTPase, whereas caspase-1 engages the Slingshot phosphatase
Hyperactive dendritic cells induce potent adaptive immune responses and are elicited by caspase-11, an enzyme that binds oxidized phospholipids and bacterial lipopolysaccharide.
Caspase-1-activated IL-18 induces IFN-gamma to prime caspase-11 and rapidly clear Burkholderia thailandensis infection.
These results argue that caspase-1, -4 or -5 can be recruited to inflammasomes under specific circumstances, often leading to distinctly organized and localized complexes that may impact the functions of these proteases
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.
, apoptotic cysteine protease Mih1/TX
, caspase 4, apoptosis-related cysteine protease
, protease ICH-2
, protease TX
, caspase 11
, caspase 4
, caspase 13
, evolutionary related interleukin-1-beta-converting enzyme
, IL-1 beta-converting enzyme
, caspase-1/caspase-4 hybrid
, interleukin-1 beta convertase
, interleukin-1 beta-converting enzyme
, caspase 11, apoptosis-related cysteine peptidase
, caspase 11, apoptosis-related cysteine protease
, caspase-11 short form splicing
, protease ICH-3
, caspase 1, apoptosis-related cysteine peptidase (interleukin 1, beta, convertase)
, caspase 4, apoptosis-related cysteine peptidase