Target intelligence / Profile preview

Caspase recruitment domain family member 16 (CARD16)

Target
CARD16
Molecular classification
Protein with caspase recruitment domain (CARD), Caspase inhibitor, Protease inhibitor complex component, Regulatory protein (regulator of procaspase-1), CARD-only protein (COP)
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Overview

Caspase recruitment domain family member 16 (CARD16), commonly abbreviated as CARD16 or COP, is a regulatory protein belonging to the CARD-only proteins (COPs) with inhibitor functions for caspase-1 and caspase-4 activation. CARD16 regulates the proteolytic maturation and release of the pro-inflammatory cytokine interleukin-1 beta (IL-1β) in response to inflammatory stimuli, such as lipopolysaccharide, by controlling the assembly and activity of caspase-1 protein complexes. CARD16 can form oligomers that interact with caspase-1 and modulate cell death in multiple cell types, serving anti-apoptotic and anti-inflammatory roles. It participates in the regulation of signal transduction and gene expression related to inflammatory and stress responses. CARD16 also plays a role in disease, such as restraining apoptosis in cancer cells, contributing to inflammation, and buffering neuronal cells from death in neurodegenerative conditions like Huntington's disease.

Other names
COPCOP1Pseudo-ICEPseudo-IL1B-converting enzymeCaspase recruitment domain-containing protein 16CARD-only protein 1Caspase recruitment domain-only protein 1Caspase-1 inhibitor COPCaspase-1 dominant-negative inhibitor pseudo-ICELLID-114769
02

Mechanism of action

Inhibition of caspase-1 and caspase-4 activation, preventing cleavage of pro-IL-1β and downstream inflammation/apoptosis

03

Biological functions

Inhibition of caspase-1 and caspase-4 activationNegative regulation of interleukin-1 beta (IL-1β) release and maturationRegulation of cell death and apoptosisCellular response to lipopolysaccharideRegulation of gene expression and signal transductionModulation of NF-kappa-B activation (during pro-inflammatory cytokine response)
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Disease associations

Cancer (including glioma and mandibular cancer)Metabolic dysfunction and alcohol-associated liver diseaseInflammationNeurodegenerative disease (e.g., Huntington’s disease)
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Safety considerations

Therapeutic challenges may arise from modulation of cell death pathways, as excessive inhibition of caspase activity can impair host defense and drive cancer; conversely, insufficient inhibition promotes unwanted cell death and inflammation

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