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正常/肿瘤
colorectal, gastric, and endometrial carcinoma
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Lymphocyte Stimulation
peptide
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NCBI Gene SummaryNCBI
This gene encodes 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 two subunits, large and small, that dimerize to form the active enzyme. Overexpression of the active form of this enzyme induces apoptosis in fibroblasts. Max, a central component of the Myc/Max/Mad transcription regulation network important for cell growth, differentiation, and apoptosis, is cleaved by this protein; this process requires Fas-mediated dephosphorylation of Max. The expression of this gene is regulated by interferon-gamma and lipopolysaccharide. Alternatively spliced transcript variants have been identified for this gene. [provided by RefSeq, Aug 2010].
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GeneCards Summary
CASP5 (Caspase 5) is a Protein Coding gene. Diseases associated with CASP5 include Cowpox and Familial Mediterranean Fever. Among its related pathways are RIPK1-mediated regulated necrosis and p53 Signaling. Gene Ontology (GO) annotations related to this gene include cysteine-type endopeptidase activity and scaffold protein binding. An important paralog of this gene is CASP4.
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UniProtKB SwissProt Summary
Thiol protease that acts as a mediator of programmed cell death . Initiates pyroptosis, a programmed lytic cell death pathway through cleavage of Gasdermin-D (GSDMD): cleavage releases the N-terminal gasdermin moiety (Gasdermin-D, N-terminal) that binds to membranes and forms pores, triggering pyroptosis . During non-canonical inflammasome activation, cuts CGAS and may play a role in the regulation of antiviral innate immune activation. ( CASP5_HUMAN,P51878 ).
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引用文献
[1].Schwitalle Y, Linnebacher M, Ripberger E, Gebert J, von Knebel Doeberitz M. Immunogenic peptides generated by frameshift mutations in DNA mismatch repair-deficient cancer cells. 2004 January.
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