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Nlrp1b (基因名), NACHT, LRR and PYD domains-containing protein 1b allele 1 (蛋白名), nl1b1_mouse.
产品名称:

Mouse Nlrp1b/ NACHT, LRR and PYD domains-containing protein 1b allele 1 ELISA Kit

货号:

E15885m

商标:
EIAab®
监管等级:
别名:

Nalp1b

检测方法:
ELISA
特异性:
Natural and recombinant mouse NACHT, LRR and PYD domains-containing protein 1b allele 1
样品类型:
Serum, plasma, tissue homogenates, cell culture supernates and other biological fluids
样品数据:
研究领域:
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Mouse Nlrp1b ELISA Kit
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Mouse Nlrp1b ELISA Kit
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产品说明书
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通用注释


亚单元:
Sensor component of NLRP1 inflammasomes. Inflammasomes are supramolecular complexes that assemble in the cytosol in response to pathogens and other damage-associated signals and play critical roles in innate immunity and inflammation. Classical inflammasomes consist of a signal sensor component, an adapter (ASC/PYCARD), which recruits an effector proinflammatory caspase (CASP1 and possibly CASP4/CASP11). CASP1 filament formation increases local enzyme concentration, resulting in trans-autocleavage and activation. Active CASP1 then processes IL1B and IL18 precursors, leading to the release of mature cytokines in the extracellular milieu and inflammatory response. In NLRP1 inflammasome, the role of PYCARD is not clear. Following activation, Nlrp1b may directly interact with CASP1 (through the CARD domain) to form a functional inflammasome (PubMed:19124602, PubMed:19651869, PubMed:24492532). Hence PYCARD may not be necessary for NLRP1 and CASP1 interaction, but is required for speck formation and full inflammasome activity (PubMed:19651869, PubMed:24492532). Homomer (PubMed:19651869, PubMed:22536155). Interacts (via LRR repeats) with BCL2 and BCL2L1 (via the loop between motifs BH4 and BH3); these interactions reduce NLRP1 inflammasome-induced CASP1 activation and IL1B release, possibly by impairing NLRP1 interaction with PYCARD (By similarity). Interacts with NOD2; this interaction may increase IL1B release (By similarity). Interacts with EIF2AK2/PKR; this interaction requires EIF2AK2 activity, is accompanied by EIF2AK2 autophosphorylation and promotes inflammasome assembly in response to Bacillus anthracis lethal toxin (PubMed:22801494). Interacts with MEFV; this interaction targets NLRP1 to degradation by autophagy, hence preventing excessive IL1B- and IL18-mediated inflammation.


功能:
As the sensor component of the NLRP1 inflammasome, plays a crucial role in innate immunity and inflammation. In response to pathogens and other damage-associated signals, initiates the formation of the inflammasome polymeric complex, made of Nlrp1b, CASP1, and possibly PYCARD. Recruitment of proCASP1 to the inflammasome promotes its activation and CASP1-catalyzed IL1B and IL18 maturation and secretion in the extracellular milieu. Activation of NLRP1 inflammasome is also required for HMGB1 secretion. The active cytokines and HMGB1 stimulate inflammatory responses. Inflammasomes can also induce pyroptosis, an inflammatory form of programmed cell death (PubMed:19651869, PubMed:21170303, PubMed:22753929, PubMed:22536155, PubMed:23818853). Activated by cleavage by Bacillus anthracis lethal toxin (LT) endopeptidase component (PubMed:19124602, PubMed:19651869, PubMed:19949100, PubMed:22536155, PubMed:23818853,PubMed:24935976, PubMed:24492532). Activated by metabolic inhibitors, such as 2-deoxy-D-glucose and sodium azide, by nutrient deprivation and hypoxia, possibly due to a decrease in cytosolic ATP (PubMed:23230290, PubMed:24935976). Also activated by Toxoplasma gondii (PubMed:24218483). Not activated by muramyl dipeptide, nor by full-length bacterial peptidoglycan (PubMed:22753929). Primary mediator of macrophage susceptibility to LT. In response to Bacillus anthracis infection, macrophages and dendritic cells release IL1B and undergo pyroptosis, an inflammatory form of programmed cell death. This early inflammatory response to the toxin increases resistance to infection by B. anthracis spores (PubMed:16429160, PubMed:19949100, PubMed:21170303, PubMed:22753929, PubMed:23818853). Binds ATP.


亚细胞位置:
Cytoplasm Cytoplasm Cytosol Inflammasome Membrane


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