SLC17A9 (gene): Difference between revisions

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==Function==
==Function==


This gene encodes a member of a family of transmembrane proteins that are involved in the transport of small molecules. The encoded protein participates in the vesicular uptake, storage, and secretion of adenoside triphosphate (ATP) and other nucleotides. A mutation in this gene was found in individuals with autosomal dominant disseminated superficial actinic porokeratosis-8. Alternative splicing results in multiple transcript variants.
This gene encodes a member of a family of [[Transmembrane protein|transmembrane proteins]] that are involved in the transport of [[Small molecule|small molecules]]. The encoded protein participates in the vesicular uptake, storage, and secretion of [[Adenosine triphosphate|adenoside triphosphate]] (ATP) and other [[Nucleotide|nucleotides]]. A [[mutation]] in this gene was found in individuals with autosomal dominant [[Disseminated superficial actinic porokeratosis|disseminated superficial actinic porokeratosis-8]]. Alternative splicing results in multiple [[transcript variants]].


== References ==
== References ==
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Revision as of 14:29, 9 March 2018


VALUE_ERROR (nil)
Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

n/a

Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

Solute carrier family 17 member 9 is a protein that in humans is encoded by the SLC17A9 gene. [1]

Function

This gene encodes a member of a family of transmembrane proteins that are involved in the transport of small molecules. The encoded protein participates in the vesicular uptake, storage, and secretion of adenoside triphosphate (ATP) and other nucleotides. A mutation in this gene was found in individuals with autosomal dominant disseminated superficial actinic porokeratosis-8. Alternative splicing results in multiple transcript variants.

References

  1. "Entrez Gene: Solute carrier family 17 member 9". Retrieved 2016-07-27.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.