Recombinant Mouse CHIT1 Protein Standard (His tag)

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CHIT1 or chitotriosidase is a glycosyl hydrolase enzyme with significant roles in chitin breakdown. It has an approximate mass of 50 kDa and recognizes chitin-containing substances. CHIT1 predominantly expresses in macrophages and acts as an important enzyme in innate immunity by degrading pathologically accumulated chitin. Alternative names for CHIT1 include chitinase-1 and it is distinguishable by its active role in neutralizing fungal pathogens utilizing this chitinase mechanism.

Biological function summary

CHIT1 participates in inflammatory processes and helps in tissue remodeling which is important in immune responses. CHIT1 does not typically form part of a complex but operates independently to mediate macrophage response through its chitinase activity. It handles polysaccharide elements in cellular debris impacting macrophage activation states. Macrophages utilize CHIT1 to counteract foreign bodies engulfed during phagocytosis playing essential roles in managing fungal infections.

Pathways

CHIT1 influences both the immune response and metabolic pathways through its enzyme function. One key pathway involving CHIT1 is the mannose receptor-mediated clearance pathway which clears glycoproteins from systemic circulation. CHIT1 activity mirrors that of other chitinases like AMCase although they derive from separate genetic backgrounds. CHIT1 contribution enhances macrophage functionality within phagolysosomal pathways important for broad-spectrum pathogen eradication.

CHIT1 correlates significantly with Gaucher's disease and chronic obstructive pulmonary disease (COPD). In Gaucher's disease elevated CHIT1 levels serve as a biomarker indicating macrophage activation and infiltration. In the case of COPD CHIT1 modulates inflammatory responses that contribute to disease progression and respiratory complications. CHIT1 interacts with proteins associated with immune regulation such as TNF-alpha in these diseases impacting inflammatory pathways and disease severities.