SLC17A4 Back

solute carrier family 17 (sodium phosphate), member 4

External References:      Wikipedia GeneCards HUGO COSMIC Google Scholar

NCBI Description of SLC17A4
Phosphate homeostasis is maintained by regulating intake, intestinal absorption, bone deposition and resorption, and renal excretion of phosphate. The central molecule in the control of phosphate excretion from the kidney is the sodium/phosphate cotransporter NPT1 (SLC17A1; MIM 182308), which is located in the renal proximal tubule. NPT1 uses the transmembrane electrochemical potential gradient of sodium to transport phosphate across the cell membrane. SLC17A4 is a similar sodium/phosphate cotransporter in the intestinal mucosa that plays an important role in the absorption of phosphate from the intestine (summary by Shibui et al., 1999 [PubMed 10319585]).[supplied by OMIM, Feb 2011].

Community Annotation of SLC17A4 Add / Edit SLC17A4: Annotations

No community annotations yet for SLC17A4.
Sort mutations by: Tumor type  Mutation type  Position  
Straightedge cursor Expand

Figure notes


• "Mouse over" a mutation to see details.
• Missense green saturation indicates evolutionary conservation of the mutated positions.
• Red hashes in protein strip are splice sites.
• Blue-white-red bars are log2 copy ratio distributions (–1 to +1) from Zack et al. (2013).


Legend

SLC17A4 is highly significantly mutated in
(none)
SLC17A4 is significantly mutated in
(none)
SLC17A4 is near significance in
(none)

Click on a tumor type to see its full list of significant genes.

Data details


• Mutation list for SLC17A4