Caspases are cysteine proteases that cleave C-terminal aspartic acid residues on their substrate molecules. Caspase-12 (CASP12) process inflammatory cytokines. It attenuates the macrophage-elicited T helper cell type 1 and type 2 cytokine response, with probable compensatory enabling of T cell-derived interferon-gamma formation. Caspase-12 dampened the production of the proinflammatory cytokines interleukin 1-beta, IL-18 and IFNg, but not tumor necrosis factor-alpha and IL-6, in response to various bacterial components that stimulate Toll-like receptor and NOD pathways. In rodents, Casp12 mediates apoptosis in response to endoplasmic reticulum stress. However, in human, Caspase-12 appears to be nonfunctional. A SNP in Caspase-12 in humans results in the synthesis of either a truncated protein (Csp12S) or a full-length caspase proenzyme (Csp12L). SNP encoding Csp12L is confined to populations of African descent and confers hyporesponsiveness to lipopolysaccharide-stimulated cytokine production in ex vivo whole blood but has no significant effect on apoptotic sensitivity. PCR analysis detected highest expression of Caspase-12 in lung. Expression was intermediate in small intestine, stomach, and kidney. Nine Caspase-12 splice variants are identified in lung and small intestine.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Protein Aliases: CASP-12; CASP12P1; caspase 12 pseudogene 1; Inactive caspase-12; UNQ9415
Gene Aliases: CASP-12; CASP12; CASP12P1; UNQ9415/PRO34398
UniProt ID: (Human) Q6UXS9
Entrez Gene ID: (Human) 100506742