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CASP5 — NLRP1

Pathways - manually collected, often from reviews:

• KEGG NOD-like receptor signaling pathway: NLRP1 → CASP5 (protein-protein, binding/association)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Hprd Interaction: NLRP1 — CASP5 (in vivo) Martinon et al., Mol Cell 2002*, Bruey et al., Cell 2007*
• IRef Hprd Interaction: NLRP1 — CASP5 (in vitro) Martinon et al., Mol Cell 2002*, Bruey et al., Cell 2007*
• IRef Hprd Interaction: Complex of 33 proteins (in vivo) Martinon et al., Mol Cell 2002*
• IRef Intact Interaction: CASP5 — NLRP1 (physical association, anti tag coimmunoprecipitation) Bruey et al., Cell 2007*
• IRef Ophid Interaction: CASP5 — NLRP1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Squires et al., J Biol Chem 2007 (Necrosis) : Activation of caspase-1 through the inflammasome protein Nalp1b controls anthrax lethal toxin ( LT ) -induced necrosis in murine macrophages
Frederick Lo et al., Biochem Biophys Res Commun 2008 (Brain Injuries) : In addition, transient expression of recombinant NALP1 or NALP5 in neurons induced caspase-3 activation and apoptosis ... These data suggest that NALP1 and NALP5 may regulate caspase activation and apoptosis in injured neurons, and thus represent novel molecular targets for therapeutic intervention in neurodegenerative disorders
Reig et al., Cell Microbiol 2008 : Macrophages from certain inbred mice strains undergo rapid death upon LT treatment mediated by caspase-1 activation dependent on Nalp1b , an inflammasome component
Faustin et al., Proc Natl Acad Sci U S A 2009 (Inflammation) : Bcl-2 and Bcl-X ( L ) inhibited caspase-1 activation induced by NLRP1 in a concentration dependent manner, with K ( i ) approximately 10 nM
Li et al., Pain 2009 (Complex Regional Pain Syndromes...) : Using this model we observed that : ( 1 ) inflammasome components and products NALP1, caspase-1, IL-1beta and IL-18 were present in low levels in normal skin, but expression of all these was strongly up-regulated after fracture, ( 2 ) NALP1 , caspase-1 and IL-1beta were co-expressed in keratinocytes, and the number of NALP1, caspase-1 , and IL-1beta positive cells dramatically increased at 4 weeks post-fracture, ( 3 ) LY303870, an NK1 receptor antagonist, effectively blocked fracture induced up-regulation of activated inflammasome components and cytokines, ( 4 ) IL-1beta and IL-18 intraplantar injection induced mechanical allodynia in normal rats, and ( 5 ) both a selective caspase-1 inhibitor and an IL-1 receptor antagonist attenuated fracture induced hindpaw mechanical allodynia
Hedl et al., Am J Physiol Gastrointest Liver Physiol 2013 (Crohn Disease...) : Importantly, we find that, during chronic Nod2 stimulation, NLRP3/NLRP1 inflammasome mediated caspase-1 activation with subsequent IL-1 secretion is essential for the subsequent bifurcation to downregulated proinflammatory cytokines and upregulated bacterial killing
Faustin et al., Methods Mol Biol 2013 : Protocols are provided for : ( a ) expression and purification of inflammasome core components ( NLRP1 and pro-caspase-1 proteins ) using the baculovirus/insect cell expression system, and ( b ) functional monitoring of NLRP1 mediated caspase-1 activation in response to NLRP1 ligand muramyl dipeptide ( MDP ) and ATP