SCUBA

MCOLN2 — Mucolipin TRP cation channel 2

MCOLN2 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.

MCOLN2's module in each cell type

Cell typeModuleShares the module with
CD19⁺ B cellsBCR Ras signaling
BCR/AP1/NFKb pathway
ANKRD28, CCL5, DOK3, GSTK1, GYPC, HOPX, HSH2D, ITGAM +12 moreView in SCUBA
CD4⁺ T cellsTh17 lineage
Th17 fate
ADA, ARHGEF3, CD226, CD52, DENND3, EVL, IDH2, IL17RE +13 moreView in SCUBA
Gamma-delta T cellsNK-like Mature gd-T
cytotoxicity
ABHD2, ATG9A, CEP78, HAVCR2, HSH2D, IFIT2, ITGAX, KIR2DL1 +14 more

About the gene

SynonymsFLJ36691, TRP-ML2, TRPML2
Chromosome1: 84925583-84997113
Predicted locationMembrane
Essential geneNo
Protein classPredicted membrane proteins, Transporters, Voltage-gated ion channels
Molecular functionCalcium channel, Ion channel
Biological processAdaptive immunity, Calcium transport, Immunity, Innate immunity, Ion transport, Protein transport, Transport

Function

Nonselective cation channel probably playing a role in the regulation of membrane trafficking events. Acts as a Ca(2+)-permeable cation channel with inwardly rectifying activity. May activate ARF6 and be involved in the trafficking of GPI-anchored cargo proteins to the cell surface via the ARF6- regulated recycling pathway. May play a role in immune processes. In adaptive immunity, TRPML2 and TRPML1 may play redundant roles in the function of the specialized lysosomes of B cells (By similarity). In the innate immune response, may play a role in the regulation of chemokine secretion and macrophage migration (By similarity). Through a possible and probably tissue-specific heteromerization with MCOLN1 may be at least in part involved in many lysosome-dependent cellular events. Also functions as a Fe(2+) permeable channel (By similarity).

Human Protein Atlas · Open Targets · UniProt

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