Nlrp1b

Summary

Gene Symbol: Nlrp1b
Description: NLR family, pyrin domain containing 1B
Alias: NACHT, LRR and PYD domains-containing protein 1b allele 3-like, NLR family, pyrin domain containing 1B
Species: rat
Products:     Nlrp1b

Top Publications

  1. Bouchier Hayes L, Conroy H, Egan H, Adrain C, Creagh E, MacFarlane M, et al. CARDINAL, a novel caspase recruitment domain protein, is an inhibitor of multiple NF-kappa B activation pathways. J Biol Chem. 2001;276:44069-77 pubmed
    ..Thus, CARDINAL is a novel regulator of NF-kappaB activation in the context of pro-inflammatory signals. ..
  2. Chavarria Smith J, Vance R. Direct proteolytic cleavage of NLRP1B is necessary and sufficient for inflammasome activation by anthrax lethal factor. PLoS Pathog. 2013;9:e1003452 pubmed publisher
    ..Here we determine the mechanism of activation of the NLRP1B inflammasome in mice...
  3. Razmara M, Srinivasula S, Wang L, Poyet J, Geddes B, DiStefano P, et al. CARD-8 protein, a new CARD family member that regulates caspase-1 activation and apoptosis. J Biol Chem. 2002;277:13952-8 pubmed
    ..Overexpression of CARD-8 can also induce apoptosis in transfected cells. The results suggest that CARD-8 represents a new signaling molecule involved in the regulation of caspase-1 and NF-kappaB activation. ..
  4. Stilo R, Leonardi A, Formisano L, Di Jeso B, Vito P, Liguoro D. TUCAN/CARDINAL and DRAL participate in a common pathway for modulation of NF-kappaB activation. FEBS Lett. 2002;521:165-9 pubmed
    ..Thus, our observations suggest that DRAL and TUCAN/CARDINAL may participate in a regulatory mechanism that coordinates cellular responses controlled by NF-kappaB transcription factor. ..
  5. Agostini L, Martinon F, Burns K, McDermott M, Hawkins P, Tschopp J. NALP3 forms an IL-1beta-processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder. Immunity. 2004;20:319-25 pubmed
    ..Macrophages from Muckle-Wells patients spontaneously secrete active IL-1beta. Increased inflammasome activity is therefore likely to be the molecular basis of the symptoms associated with NALP3-dependent autoinflammatory disorders. ..