SCUBA

CHI3L1 — Chitinase 3 like 1

CHI3L1 belongs to a gene co-expression module in 3 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

CHI3L1's module in each cell type

Cell typeModuleShares the module with
FibroblastsInflammatory ECM Remodeling
ECM remodeling
ABRACL, ADAMTS2, CD82, COTL1, GGCT, LXN, MT2A, NID2 +5 moreView in SCUBA
MacrophagesSPP1 Tissue Remodeling
ECM remodeling
BST1, CD52, CHIT1, CSF1, FBP1, FGR, FN1, GCHFR +19 moreView in SCUBA
NeutrophilsSecondary Granule Antibacterial
Degranulation
CAMP, CHIT1, CRISP3, CYBB, HP, LCN2, LTF, MMP8 +3 more

About the gene

SynonymsGP39, YK-40, YKL40
Chromosome1: 203178931-203186704
Predicted locationIntracellular, Secreted
Essential geneNo
Protein classCancer-related genes, Disease related genes, Human disease related genes, Metabolic proteins, Plasma proteins, Predicted intracellular proteins, Predicted secreted proteins
Molecular functionAntimicrobial
Biological processApoptosis, Inflammatory response

Function

Carbohydrate-binding lectin with a preference for chitin. Has no chitinase activity. May play a role in tissue remodeling and in the capacity of cells to respond to and cope with changes in their environment. Plays a role in T-helper cell type 2 (Th2) inflammatory response and IL-13-induced inflammation, regulating allergen sensitization, inflammatory cell apoptosis, dendritic cell accumulation and M2 macrophage differentiation. Facilitates invasion of pathogenic enteric bacteria into colonic mucosa and lymphoid organs. Mediates activation of AKT1 signaling pathway and subsequent IL8 production in colonic epithelial cells. Regulates antibacterial responses in lung by contributing to macrophage bacterial killing, controlling bacterial dissemination and augmenting host tolerance. Also regulates hyperoxia- induced injury, inflammation and epithelial apoptosis in lung.

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.