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抗Rat (Rattus) Caspase 2 抗体:
抗Mouse (Murine) Caspase 2 抗体:
抗Human Caspase 2 抗体:
Human Polyclonal Caspase 2 Primary Antibody for WB - ABIN3043696
Jiang, Li, Zhou, Wang, Zhang, Wang: Colistin-induced apoptosis in PC12 cells: involvement of the mitochondrial apoptotic and death receptor pathways. in International journal of molecular medicine 2014
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Human Polyclonal Caspase 2 Primary Antibody for IHC (fro), WB - ABIN550327
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 2 Primary Antibody for IHC, WB - ABIN222882
Basu, Adkins, Basu: Down-regulation of caspase-2 by rottlerin via protein kinase C-delta-independent pathway. in Cancer research 2008
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caspase-2 has a role as an initiator caspase (显示 CASP3 抗体) in lipoapoptosis
tail regression at metamorphosis implicates an apoptotic pathway inducible by T(3) hormone in an organ autonomous manner and involving the cell death executioners BH3 interacting domain death agonist (显示 BID 抗体) and Caspases-2 and -8
Caspase-2 phosphorylated at S135 binds 14-3-3zeta (显示 YWHAZ 抗体), thus preventing C2 dephosphorylation.
The data demonstrate that cell death is prevented during mitosis through the inhibitory phosphorylation of caspase-2 and suggest that under conditions of mitotic arrest, cdk1 (显示 CDK1 抗体)-cyclin B1 (显示 CCNB1 抗体) activity must be overcome for apoptosis to occur.
A novel function for caspase-2 in myocyte differentiation and myogenesis.
Casp2(-/-) mice, which are more susceptible to genomic instability, are limited in their ability to respond to DNA damage and thus carry more damaged cells resulting in accelerated tumourigenesis.
BECN1/Beclin 1 (显示 BECN1 抗体) binding to viral phosphoprotein (P) induced an incomplete autophagy via activating the pathways CASP2-AMPK (显示 PRKAA1 抗体)-AKT (显示 AKT1 抗体)-MTOR (显示 FRAP1 抗体) and CASP2-AMPK (显示 PRKAA1 抗体)-MAPK (显示 MAPK1 抗体) by decreasing CASP2.
We further generated Casp2(C320S) mutant mice to demonstrate that caspase-2 catalytic activity is essential for its function in limiting aneuploidy. Our results provide direct evidence that the apoptotic activity of caspase-2 is necessary for deleting cells with mitotic aberrations to limit aneuploidy
These results provide the first evidence of caspase-2 in regulating haematopoietic stem cell and progenitor differentiation, as well as aneuploidy, in vivo.
Study describes a novel pathological process in which caspase-2 cleavage of tau at Asp314 impairs cognitive and synaptic function in animal and cellular models of tauopathies by promoting the missorting of tau to dendritic spines.
Caspase-2 deficiency protected mice from diet-induced obesity, metabolic syndrome and nonalcoholic fatty liver disease.
The tumor-modulatory effects of Caspase-2 and Pidd1 do not require the scaffold protein (显示 HOMER1 抗体) Raidd (显示 CRADD 抗体)
Data show that indoles can effectively suppress acute hepatic inflammation caused by staphylococcal enterotoxin B (SEB) maybe mediated by decreased expression of miR-31 and caspase-2-dependent apoptosis in T cells.
Data indicate that the nucleotide-binding domain and leucine-rich repeat containing (显示 NLRX1 抗体) (NLRP3 (显示 NLRP3 抗体))-caspase-2 axis drives general endoplasmic reticulum (ER) stress-induced inflammasome activation.
these data identify a novel caspase-2-interacting factor, FAN (显示 NSMAF 抗体), and expand the role for the enzyme in seemingly non-apoptotic cellular mechanisms.
Results suggest that TG-induced macrophage cell death is mediated via the caspase-2.
study demonstrates that apoptosis inhibitor 5 (API5/AAC11 (显示 API5 抗体)) is an endogenous and direct inhibitor of caspase-2. API5 (显示 API5 抗体) protein directly binds to the caspase (显示 CASP3 抗体) recruitment domain (CARD) of caspase-2 and impedes dimerization and activation of caspase-2.
This peptide, Ac-VDTTD-AFC, was efficiently cleaved by purified caspase-2 and auto-activating caspase-2 in mammalian cells, and exhibited better selectivity for caspase-2 relative to caspase-3 (显示 CASP3 抗体) than reagents that are currently available.
There results support a special role for miR (显示 MLXIP 抗体)-149 in malignant glioma by targeting Caspase-2
Whole exome sequencing (WES) of an affected fetus, and subsequent Sanger sequencing of the second fetus, revealed a homozygous frameshift variant in CRADD (显示 CRADD 抗体), which encodes an adaptor protein that interacts with PIDD (显示 PIDD 抗体) and caspase-2 to initiate apoptosis
This study shows that human procaspase-2 interaction with 14-3-3 zeta (显示 YWHAZ 抗体) is governed by phosphorylation at both S139 and S164 (显示 RBM25 抗体).
NPM1 (显示 NPM1 抗体)-dependent nucleolar PIDDosome is a key initiator of the caspase-2 activation cascade.
Sensitization of colon carcinoma cells to radiation-induced cell death and DNA-damage by HuR (显示 ELAVL1 抗体) knockdown critically depends on caspase-2.
BCL9L (显示 BCL9L 抗体) dysfunction contributes to aneuploidy tolerance in both TP53 (显示 TP53 抗体)-WT and mutant cells by reducing basal caspase-2 levels and preventing cleavage of MDM2 (显示 MDM2 抗体) and BID (显示 BID 抗体).
EtOH-induced mitochondria-mediated apoptosis is initiated by caspase-2 activation, which is regulated by CoQ10
the capacity for blastocysts to undergo further development is related to degree of group II caspase (显示 CASP3 抗体) activity
Caspase-2 expression was increased two-fold in the hypoxia group. After Src kinase (显示 CSK 抗体) inhibition followed by hypoxia, caspase-2 expression was similar to normoxia levels: hypoxia results in increased expression of caspase-2 protein in the cytosolic fraction of the cerebral cortex of the newborn piglets. This increase is mediated by Src kinase (显示 CSK 抗体).
hypoxia/re-oxygenation injury in cultured proximal tubule cells induced apoptosis by activation of caspase-2, which is required for the mitochondrial translocation of Bax (显示 BAX 抗体).
This gene encodes a member of the cysteine-aspartic acid protease (caspase) family. Caspases mediate cellular apoptosis through the proteolytic cleavage of specific protein substrates. The encoded protein may function in stress-induced cell death pathways, cell cycle maintenance, and the suppression of tumorigenesis. Increased expression of this gene may play a role in neurodegenerative disorders including Alzheimer's disease, Huntington's disease and temporal lobe epilepsy. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
, ICH-1 protease
, protease ICH-1
, neural precursor cell expressed developmentally down-regulated protein 2
, protein phosphatase 1, regulatory subunit 57
, caspase 2, apoptosis-related cysteine peptidase (neural precursor cell expressed, developmentally down-regulated 2)
, ICH1 protease
, caspase 2, apoptosis-related cysteine protease
, cysteine protease caspase-2