SCUBA

PKD1 — Polycystin 1, transient receptor potential channel interacting

PKD1 belongs to a gene co-expression module in 1 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.

PKD1's module in each cell type

Cell typeModuleShares the module with
Gamma-delta T cellsEffector Cytokine Secretion
Inflammation
APBA2, ASPH, CCL3, CCL4, CMC1, CYRIA, DTHD1, DTNBP1 +25 more

About the gene

SynonymsPBP, Pc-1, TRPP1
Chromosome16: 2088708-2135898
Predicted locationIntracellular, Membrane, Secreted
Essential geneNo
Protein classDisease related genes, Human disease related genes, Plasma proteins, Potential drug targets, Predicted intracellular proteins, Predicted membrane proteins, Predicted secreted proteins, Transporters
Biological processWnt signaling pathway

Function

Component of a heteromeric calcium-permeable ion channel formed by PKD1 and PKD2 that is activated by interaction between PKD1 and a Wnt family member, such as WNT3A and WNT9B. Both PKD1 and PKD2 are required for channel activity. Involved in renal tubulogenesis. Involved in fluid- flow mechanosensation by the primary cilium in renal epithelium (By similarity). Acts as a regulator of cilium length, together with PKD2 (By similarity). The dynamic control of cilium length is essential in the regulation of mechanotransductive signaling (By similarity). The cilium length response creates a negative feedback loop whereby fluid shear-mediated deflection of the primary cilium, which decreases intracellular cAMP, leads to cilium shortening and thus decreases flow- induced signaling (By similarity). May be an ion-channel regulator. Involved in adhesive protein-protein and protein-carbohydrate interactions. Likely to be involved with polycystin-1-interacting protein 1 in the detection, sequestration and exocytosis of senescent mitochondria.

Human Protein Atlas · Open Targets · UniProt

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