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anti-Human Caspase 1 Antikörper:
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Human Monoclonal Caspase 1 Primary Antibody für IHC, IHC (p) - ABIN252521
Dorfleutner, Bryan, Talbott, Funya, Rellick, Reed, Shi, Rojanasakul, Flynn, Stehlik: Cellular pyrin domain-only protein 2 is a candidate regulator of inflammasome activation. in Infection and immunity 2007
Show all 30 Pubmed References
Human Polyclonal Caspase 1 Primary Antibody für IHC (p), WB - ABIN3044293
Xu, Liu, Zhang, Wang, Wang, Yang, Huo, Sun: Apoptosis-related protein expression in rabbits with blast brain injury following early hyperbaric oxygen therapy. in Neural regeneration research 2015
Show all 21 Pubmed References
Human Polyclonal Caspase 1 Primary Antibody für IHC (p), WB - ABIN3043221
Huang, Huang, Xiao, Yang, Lin, Diao: Kallistatin, a novel anti-angiogenesis agent, inhibits angiogenesis via inhibition of the NF-?B signaling pathway. in Biomedicine & pharmacotherapy = Biome?decine & pharmacothe?rapie 2014
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Mouse (Murine) Polyclonal Caspase 1 Primary Antibody für WB - ABIN5518669
Mao, Song, Li, Lv, Zhao, Li, Feng, Chen: 8-hydroxy-2-(di-n-propylamino)tetralin intervenes with neural cell apoptosis following diffuse axonal injury. in Neural regeneration research 2014
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Human Polyclonal Caspase 1 Primary Antibody für ICC, IF - ABIN4288002
Draganov, Gopalakrishna-Pillai, Chen, Zuckerman, Moeller, Wang, Ann, Lee: Modulation of P2X4/P2X7/Pannexin-1 sensitivity to extracellular ATP via Ivermectin induces a non-apoptotic and inflammatory form of cancer cell death. in Scientific reports 2015
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Human Polyclonal Caspase 1 Primary Antibody für IF, IP - ABIN222877
Peluffo, Bussmann, Stouffer, Tesone: Expression of caspase-2, -3, -8 and -9 proteins and enzyme activity in the corpus luteum of the rat at different stages during the natural estrous cycle. in Reproduction (Cambridge, England) 2006
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Human Polyclonal Caspase 1 Primary Antibody für IHC (p), WB - ABIN541459
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 1 Primary Antibody für IHC (p), WB - ABIN541460
Gracie, Robertson, McInnes: Interleukin-18. in Journal of leukocyte biology 2003
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Human Polyclonal Caspase 1 Primary Antibody für IF, IP - ABIN549149
Sasaki, Ikeda, Sato, Nakanuma: Decreased expression of Bmi1 is closely associated with cellular senescence in small bile ducts in primary biliary cirrhosis. in The American journal of pathology 2006
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Human Monoclonal Caspase 1 Primary Antibody für IHC (p), ELISA - ABIN560170
Choi, Stottmann, Yang, Meyers, Klingensmith: The bone morphogenetic protein antagonist noggin regulates mammalian cardiac morphogenesis. in Circulation research 2007
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GSDMD regulates the release of microparticulate active caspase 1 from monocytes essential for induction of cell death and thereby may play a critical role in sepsis-induced endothelial cell injury.
CASP1 was predicted as a downstream target of miR-377 Overexpression of miR-377 suppressed the expression of CASP1 in PC9 cells and knockdown of miR-377 increased the CASP1 expression in PC9GR cells.
Upregulation of NLRP3 and caspase-1 is observed in immunological non-responders (INR) HIV-infected patients. This could play a role in persistent immune activation that characterize INRs. Caspase-1 upregulation could induce CD4 T-cell loss via pyroptosis, contributing to unsatisfactory CD4 T-cells recovery.
Caspase-1 in Myeloid-derived suppressor cells is a direct T cell-independent mediator of tumor proliferation.
We discovered that the expression of the factors was significantly increased in pterygium and that caspase-1-dependent pyroptosis presents in both H2O2-treated HPFs and HConECs during which the expression of these factors was significantly elevated and the elevation of downstream factors IL-18 and IL-1beta was restrained after caspase-1 inhibition
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
C-terminal region of Human parainfluenza virus type 2 V interacts with the C-terminal region of caspase-1.
Caspase-1 gene expression was 2.2-3.4 times higher than in normal skin biopsy samples.
Caspase-1 regulates cellular trafficking via cleavage of the Rab7 adaptor protein RILP in cultured neoplastic epithelial cells has been reported.
ABT-737 elicited an anti-atopic dermatitis (AD) activity via suppression of caspase-1 activation in AD in vitro and in vivo models. Therefore, this study provides important information regarding the use of anticancer drugs for controlling allergic inflammatory diseases.
Cryo-EM structures of ASC and NLRC4 CARD filaments reveal a unified mechanism of nucleation and activation of caspase-1
The increased expression of NLRP3 and caspase-1 in fetal membrane and placental tissues may be associated with the development of premature rupture of membrane.
inflammasome activation and pyroptosis in human microglia and ODCs in vitro after exposure to inflammatory stimuli and demonstrate caspase-1 inhibition by the small-molecule inhibitor VX-765 in both cell types. GSDMD inhibition by siRNA transduction suppressed pyroptosis in human microglia.
Increased production of caspase-1 in the gut-associated lymphoid tissue and peripheral blood of HIV infected patients.
Low CASP1 expression is associated with prostate cancer.
These findings confirm the involvement of caspase-1 in non-classical secretion mechanisms and open novel perspectives for the extracellular function of secreted GBP-1.
this study demonstrates that the G+7/in6A and A10370-G polymorphisms of the CASP1 gene are associated with increased risk of developing acute coronary syndrome in Mexican population
After genotype calling and quality control filtering with exclusion of 3 cases and 3 controls, association analysis was performed across 76 directly genotyped SNPs in NLRP1, CARD, and CASP1 genes, adjusting for age, sex, and population stratification
Caspase-1 role in pyroptosis in glioma cells.Mir-214 regulates caspase-1 expression in glioma.
Data show that cyclic stretch activated the nucleotide-binding oligomerization domain-like receptor containing pyrin domain 1 and 3 (NLRP1 and NLRP3) inflammasomes and induced the release of IL-1beta and pyroptosis via a caspase-1-related mechanism in human periodontal ligament cells (HPDLCs).
Caspase-8 synergizes with the canonical NLRP3 inflammasome pathway to control caspase-1 processing and IL-1beta maturation, providing a regulatory role for caspase-8 in host resistance to in vivo Paracoccidioides brasiliensis infection.
results suggest that p53 may block oncogenic transformation by decreasing BCL6 stability via caspase-1 up-regulation, whereas aberrant BCL6 expression inactivates transactivation of p53 target genes, either by inhibiting p53 acetylation by p300 or repressing TP53 gene transcription. These findings have implications for B cell development and lymphomagenesis.
Ablation of caspase-1 inhibits traumatic brain injury-induced pyroptosis.
The inflammasome-caspase-1 complex thus functions as a holoenzyme that directs the location of caspase-1 activity but also incorporates an intrinsic self-limiting mechanism that ensures timely caspase-1 deactivation.
AIM2 inflammasome activates caspase-1 independent of caspase-8. Caspase-1 and caspase-8 are both upstream of caspase-3 cleavage initiated by AIM2.
caspase-1 protease activity is required for canonical IL-1 secretion, pyroptosis, and inflammasome-mediated immunity.
The H7N9 influenza A virus infection results in lethal inflammation in the mammalian host via the NLRP3-Casp1- IL1R1-expressing inflammasomes.
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.
Casp1Null mice expressed caspase-11 proteins and did not secrete IL-1beta and IL-18 or undergo pyroptosis in response to canonical NLRP3, NLRC4 or AIM2 inflammasome activators.
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.
Collectively, these results are consistent with a model whereby the type III secretion system apparatus of Pseudomonas aeruginosa activates the caspase-1-dependent inflammasome and caspase-3/7 through an ASC-dependent mechanism.
The results of this study indicated that beta-Amyloid peptide-induced caspase-1 activation, disrupts autophagy in the cortex and in the hippocampus resulting in neurodegeneration and memory loss.
caspase-1 regulates dopaminergic neuronal death in the pathogenesis of Parkinson's disease in mice via caspase-7/PARP1/AIF pathway.
RIP3-mediated activation of caspase-1 rather than necroptosis-dependent inflammation was responsible for aggressive inflammation in influenza A (H7N9) virus-infected mice.
we assessed the role of RIP3 in synergy with Caspase-1 in the induction of IL-1beta production in BMDM after either LPS/ATP or Chlamydia muridarum stimulation. The possibility of pyroptosis and necroptosis interplays and the role of RIP3 in IL-1beta production during Chlamydia muridarum infection in BMDM was investigated as well.
Studied the role of transient receptor potential melastatin 2 (TRPM2) in activating caspase-1 and caspase-1-dependent pyroptosis in mouse BMDMs. Found TRPM2 knockout caused higher caspase-1 activation and pyrotopsis.
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.
Nodakenin inhibited the mRNA expression and production of pro-inflammatory cytokines and caspase-1 activation
mmediately after hypoxia C8 and C1 follow a similar pattern of increase while long term this appears to dissociate
Src kinase mediates hypoxia-induced caspase-1 activation in the cerebral cortex of newborn piglets
endometrial expression of CASP1 and IL18 associated with pregnancy establishment; alteration of CASP1 and IL18 following premature exposure of uterus to estrogen during early pregnancy may contribute to conceptus loss between Days 15 to 18 of pregnancy
drICE and dcp-1 function in cell death redundantly. However, dying neurons in a few clusters strictly required drICE but not dcp-1, but required drICE and dcp-1 when drICE activity was reduced via hypomorphic mutation.
Drosophila corazonin-producing interneuron programmed cell death utilizes dronc, strica, dcp-1, and ice
Autophagy suppresses Dcp-1-mediated apoptotic cell death, whereas Dcp-1 positively regulates autophagy, possibly through feedback regulation.
novel characteristic morphological features of egg chambers lacking both dcp-1 and pita functions in the germline cells; suggested an essential role of dcp-1 and/or pita during mid-oogenesis
A double-mutant analysis between drICE and death caspase-1 (dcp-1), another effector caspase, reveals that some cells (type I) strictly require drICE for apoptosis, whereas other cells (type II) require either drICE or dcp-1.
Data show that the effector caspase Dcp-1 and the inhibitor of apoptosis protein Bruce function to regulate both autophagy and starvation-induced cell death in Drosophila.
HeT-A mRNA is derepressed in mRNA degradation mutants dcp1, indicating that the enzyme also aid in removing full-length transcripts and/or decay intermediates.
Bombyx mori caspase-1 plays an important role during baculovirus infection.
cBm-IAP1 is a vital negative regulator of apoptosis in BM-N cells and functions by preventing the activation and/or activity of Bm-Dronc and Bm-caspase-1.
Activation of Atg5, AIF and caspase genes in close association with different cell death events revealed the synchronized differential expression of apoptosis-associated genes in response to macroparasitism.
This gene encodes a protein which 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 which undergo proteolytic processing at conserved aspartic residues to produce 2 subunits, large and small, that dimerize to form the active enzyme. This gene was identified by its ability to proteolytically cleave and activate the inactive precursor of interleukin-1, a cytokine involved in the processes such as inflammation, septic shock, and wound healing. This gene has been shown to induce cell apoptosis and may function in various developmental stages. Studies of a similar gene in mouse suggest a role in the pathogenesis of Huntington disease. Alternative splicing results in transcript variants encoding distinct isoforms.
CASP1 nirs variant 1
, IL-1 beta-converting enzyme
, caspase 1, apoptosis-related cysteine peptidase (interleukin 1, beta, convertase)
, interleukin 1, beta, convertase
, interleukin 1-B converting enzyme
, IL-1B converting enzyme
, interleukin 1 beta-converting enzyme
, interleukin-1 beta convertase
, interleukin-1 beta-converting enzyme
, Interleukin 1beta converting enzyme
, caspase 1, apoptosis-related cysteine protease (interleukin 1, beta, convertase)
, interleukin-1 beta converting enzyme
, caspase-1/caspase-4 hybrid
, caspase 1
, death caspase-1