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FLASH GENE

Symbol

SLC26A1

contributors: mct - updated : 01-07-2016

HGNC name	solute carrier family 26 (sulfate transporter), member 1
HGNC id	10993

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

Corresponding disease	NPHL3 nephrolithiasis 3
Location	4p16.3      Physical location : 972.863 - 987.224
Synonym name	sulfate anion tranporter AT1
	sulfate/anion transporter SAT-1 protein
Synonym symbol(s)	EDM4, SAT1, SAT-1

DNA

TYPE	functioning gene
STRUCTURE	14.36 kb     6 Exon(s)

10 Kb 5' upstream gene genomic sequence study

regulatory sequence	Binding site   transcription factor
text structure	having a large number of potential cis-acting elements recognized by transcription factors
	a minimal promoter containing an AP1 site being essential for transcription

MAPPING

cloned

Y

linked

N

status

confirmed

RNA

TRANSCRIPTS	type	messenger

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed variant 2 3 splicing 1141 24.8 224 - Regeer, 2003 lacking a 5' exon and having an alternate 3' exon compared to variant 3 variant 1 3 splicing 3405 74.9 701 - Regeer, 2003 lacking an exon in the 5' UTR compared to variant 3 encoding the same protein than variant 3 variant 3 4 splicing 3673 74.9 701 - Regeer, 2003 encoding the same protein than variant 1

EXPRESSION

Type

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Digestive intestine small intestine       Homo sapiens   intestine large intestine colon     Homo sapiens   liver       moderately Homo sapiens Reproductive male system testis       Respiratory lung         Urinary kidney tubule convoluted tubule proximal tubule highly Homo sapiens

cells

System Cell Pubmed Species Stage Rna symbol Digestive enterocyte Homo sapiens Digestive hepatocyte Homo sapiens Urinary epithelial cell Homo sapiens

cell lineage
cell lines
fluid/secretion	moderately in blood

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	nine transmembrane segments
	cytoplasmic N and C termini with a sulfate transporter family motif
	an STAS domain (sulfate transporter and anti sigma antagonist)

conjugated

GlycoP

HOMOLOGY

interspecies	homolog to rattus Slc26a1 (78.5 pc)
	homolog to murine Slc26a1 (79.1 pc)

Homologene

FAMILY	sulfate/anion exchanger family
	SLC26A/SulP transporter (TC 2.A.53) family

CATEGORY

transport carrier

SUBCELLULAR LOCALIZATION	plasma membrane
text	multi-pass membrane protein

basic FUNCTION	involved in sulfate transport in exchange for HCO3 or oxalate
	characterized as an anion exchanger that transports anions by mediating electroneutral sulfate-oxalate, sulfate-bicarbonate, or oxalate-bicarbonate exchange
	mediates epithelial transport of oxalate and sulfate, and its localization in the kidney, liver, and intestine suggests that it may play a role in oxalate and sulfate homeostasis
	regulates both oxalate and sulfate homeostasis and may be critical to the development of calcium oxalate urolithiasis and hepatotoxicity
	is a basolateral membrane anion exchanger that mediates intestinal oxalate transport
	SLC26A1, SLC26A6 and SLC26A7 are novel participants in the extracellular transport of bicarbonate during enamel maturation, and that their functional roles may be achieved by forming interaction units with CFTR (pMID: 26671068)

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

active transport

text	Na+ independent sulfate transporter
	Cl- transport
	oxalate transport

PATHWAY

metabolism

signaling

a component

INTERACTION

DNA

RNA

small molecule

protein

cell & other

REGULATION

ASSOCIATED DISORDERS

corresponding disease(s)

NPHL3

Susceptibility

Variant & Polymorphism

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS

	Slc26a1-/- mice exhibit hyposulfatemia, hypersulfaturia, calcium oxalate urolithiasis, and nephrocalcinosis in the setting of hyperoxalemia and hyperoxaluria
	Sat1-deficient mice also have a phenotype of hyperoxalemia, hyperoxaluria, and calcium oxalate stones
	Slc36a1 loss in mice leads to hyperoxaluria and calcium oxalate renal stones
	hyperoxalemia in Slc26a1-/- mice was most likely caused by reduced intestinal secretion of oxalate, based on reduced oxalate transport in basolateral membrane vesicles from the distal ileum, cecum, and proximal colon