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anti-Rat (Rattus) Caspase 2 Antibodies:
anti-Mouse (Murine) Caspase 2 Antibodies:
anti-Human Caspase 2 Antibodies:
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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
Show all 27 Pubmed References
Human Monoclonal Caspase 2 Primary Antibody for IF, WB - ABIN968323
Guo, Srinivasula, Druilhe, Fernandes-Alnemri, Alnemri: Caspase-2 induces apoptosis by releasing proapoptotic proteins from mitochondria. in The Journal of biological chemistry 2002
Show all 5 Pubmed References
Human Monoclonal Caspase 2 Primary Antibody for IF, WB - ABIN968324
Li, Chen, Sinogeeva, Gorospe, Wersto, Chrest, Barnes, Liu: Arsenic trioxide promotes histone H3 phosphoacetylation at the chromatin of CASPASE-10 in acute promyelocytic leukemia cells. in The Journal of biological chemistry 2002
Show all 5 Pubmed References
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
Show all 2 Pubmed References
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
Show all 3 Pubmed References
caspase-2 has a role as an initiator caspase (show CASP3 Antibodies) 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 (show BID Antibodies) and Caspases-2 and -8
Caspase-2 phosphorylated at S135 binds 14-3-3zeta (show YWHAZ Antibodies), 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 (show CDK1 Antibodies)-cyclin B1 (show CCNB1 Antibodies) activity must be overcome for apoptosis to occur.
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 (show BECN1 Antibodies) binding to viral phosphoprotein (P) induced an incomplete autophagy via activating the pathways CASP2-AMPK (show PRKAA1 Antibodies)-AKT (show AKT1 Antibodies)-MTOR (show FRAP1 Antibodies) and CASP2-AMPK (show PRKAA1 Antibodies)-MAPK (show MAPK1 Antibodies) 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 (show HOMER1 Antibodies) Raidd (show CRADD Antibodies)
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 (show NLRX1 Antibodies) (NLRP3 (show NLRP3 Antibodies))-caspase-2 axis drives general endoplasmic reticulum (ER) stress-induced inflammasome activation.
these studies elucidate a Caspase-2-p53 (show TP53 Antibodies) signaling network that impacts lung tumorigenesis and chemotherapy response in vivo.
Whole exome sequencing (WES) of an affected fetus, and subsequent Sanger sequencing of the second fetus, revealed a homozygous frameshift variant in CRADD (show CRADD Antibodies), which encodes an adaptor protein that interacts with PIDD (show PIDD Antibodies) and caspase-2 to initiate apoptosis
This study shows that human procaspase-2 interaction with 14-3-3 zeta (show YWHAZ Antibodies) is governed by phosphorylation at both S139 and S164 (show RBM25 Antibodies).
NPM1 (show NPM1 Antibodies)-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 (show ELAVL1 Antibodies) knockdown critically depends on caspase-2.
BCL9L (show BCL9L Antibodies) dysfunction contributes to aneuploidy tolerance in both TP53 (show TP53 Antibodies)-WT and mutant cells by reducing basal caspase-2 levels and preventing cleavage of MDM2 (show MDM2 Antibodies) and BID (show BID Antibodies).
CASP2 down-regulation had a reverse relationship with miR (show MLXIP Antibodies)-383 down-regulation in regulating epithelial ovarian cancer development.
Results suggest that mutations at all three cleavage sites of caspase-2 protein neither affect the macromolecular core complex assembly, nor modify caspase-2 activity upon DNA damage. Consequently, caspase-2 activation occurs in the macromolecular complex without its dissociation.
These findings indicate that miR (show MLXIP Antibodies)-125a-5p decreases after HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.
We have also demonstrated that these correlations are tissue specific being reduced (CASP9 (show CASP9 Antibodies) and CASP10 (show CASP10 Antibodies)) or different (CASP2) in the liver
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 (show CASP3 Antibodies) activity
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 (show BAX Antibodies).
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