Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human SLC26A1 Antibodies:
anti-Rat (Rattus) SLC26A1 Antibodies:
Go to our pre-filtered search.
Human Polyclonal SLC26A1 Primary Antibody for ICC, IF - ABIN4354198
Gee, Jun, Braun, Lawson, Halbritter, Shril, Nelson, Tan, Stein, Wassner, Ferguson, Gucev, Sayer, Milosevic, Baum, Tasic, Lee, Hildebrandt: Mutations in SLC26A1 Cause Nephrolithiasis. in American journal of human genetics 2016
SLC26A1 L348P was associated with lower whole-body bone mineral density (BMD) and higher serum calcium, consistent with the osteochondrodysplasia exhibited by dogs and sheep with naturally occurring, homozygous, loss-of-function mutations in Slc13a1
Human SLC26A1 resembles SLC26 paralogs in its inhibition.
Mutations in SLC26A1 gene is associated with Nephrolithiasis.
Screened the SLC26A1 gene in a cohort of 13 individuals with recurrent calcium oxalate urolithiasis, which is the commonest type. DNA sequence analyses showed missense mutations in seven patients.
SLC26A1 protein,point mutation is highly responsible for the hearing loss of newborns.
The oxalate precursor glyoxylate was identified as a substrate of sat-1. Upregulated expression of sat-1 mRNA and of sat-1 protein indicates that glyoxylate may be responsible for the elevated oxalate release from hepatocytes observed in hyperoxaluria.
Characterization of the SAT1 gene and protein function.
The expression of three messengers coding for SAT-1, SAT-2 and GalNAcT-1 in human samples of intestinal cancer and some cell lines (breast cancer and melanomas), was evaluated.
No mutation was found in the coding regions and intron-exon boundaries of the genes for CA II, CA IV, CA XIV, kNCB1, NHE3, NHE8, NHRF1, NHRF2 and SLC26A6 amplified from genomic DNA of family members with pRTA.
Slc26a1, Slc26a6 and Slc26a7 are novel participants in the extracellular transport of bicarbonate during enamel maturation.
study concludes that a DIDS-sensitive basolateral transporter is involved in mediating oxalate secretion across mouse duodenum, but Sat1 itself is dispensable for this process
Sat1 regulates both oxalate and sulfate homeostasis and may be critical to the development of calcium oxalate urolithiasis and hepatotoxicity.
first characterization of the structure and regulation of the Sat1 gene encoding a SO(4)(2-)/chloride/oxalate anion transporter
This gene is a member of a family of sulfate/anion transporter genes. Family members are well conserved in their genomic (number and size of exons) and protein (aa length among species) structures, but have markedly different tissue expression patterns. This gene is primarily expressed in the liver, pancreas, and brain. Three splice variants that encode different isoforms have been identified.
solute carrier family 26 (sulfate transporter), member 1
, SLC26A1 anion exchanger
, sulfate anion transporter 1
, sulfate anion transporter 1-like
, sulfate anion tranporter AT1
, sulfate/anion transporter SAT-1 protein
, canalicular sulfate transporter
, solute carrier family 26 member 1
, sulfate/carbonate antiporter
, solute carrier family 26, member 1
, sulfate anion transporter-1