Disease relevance of SLC26A1

• Between 1989 and 1992, 7970 wild ungulates, comprising 14 different species, were tested for antibodies to types SAT 1, SAT 2 and SAT 3 foot-and-mouth disease (FMD) virus [1].
• The different ganglioside distribution seems to correlate with the tumour size; (3), Sarcoma Galliera-strain cells SGS/3A and normal syngenic murine fibroblasts FG: transformed cells exhibit a lower activity of sialyltransferases (SAT-1, SAT-2, SAT-4) compared to normal fibroblasts, suggesting a possible correlation with the ganglioside pattern [2].

High impact information on SLC26A1

• A chimera that was composed of the amino terminal fragment of SLC26A7 and the carboxyl terminal fragment of SLC26A1, and a C-terminal-truncated SLC26A7 were retained in the cytoplasm in hypertonicity [3].
• The sulfate-anion antiporter 1 (SAT-1; hsat-1) may also contribute to organic anion transport at the basolateral membrane [4].
• Progressive increases in the activities of SAT-1 and SAT-3 were detected in lymphocytes stimulated with PHA, whereas no increase was observed in control lymphocytes incubated in culture medium alone [5].
• Although the sulfate/anion transporter (sat-1; SLC26A1) was isolated from a rat liver cDNA library by expression cloning, localization of sat-1 within the liver and its contribution to the transport of sulfate and organo sulfates have remained unresolved [6].
• To study this further, NaSi-1 (SLC13A1) and Sat-1 (SLC26A1) gene structures were determined and recent studies have characterized their respective gene promoters [7].

Biological context of SLC26A1

• We report the expansion of the SLC26 family with five new members in chromosomes 3, 6, 8, 12, and 17 and mapping of SLC26A1 to 4p16 [8].
• Using SAT1 5' flanking region truncations, the first 135 bp was shown to be sufficient for basal promoter activity [9].
• The SAT1 gene is comprised of four exons stretching 6 kb in length, with an alternative splice site formed from an optional exon [9].
• The sat1 gene, which confers resistance to streptothricin, an antimicrobial that has never been approved for use in the United States, was identified in integrons from three (7%) of the isolates [10].
• Twelve different values of control flow (Qctr) were measured (Qmsr) using 3 different cardiac output computers (Abbott Critical Care System, Oximetrix 3 SvO2/CO Computer, Baxter Oximeter/Cardiac Output Computer SAT-1; American Edwards Laboratories, 9520 A Cardiac Output Computer) [11].

Anatomical context of SLC26A1

• SAT1 5' flanking region led to promoter activity in renal OK and LLC-PK1 cells [9].
• Intact lymphocytes were needed for the lectin-stimulated increase of sialyltransferase activities because neither concanavalin A nor phytohemagglutinin added to the broken cell preparation modulated SAT-1 activity [5].
• DESIGN: Values of SvO2 recorded by three pulmonary artery catheters for continuous monitoring, SAT1, SAT2 and Oximetrix3 (OX3), were compared in a prospective manner to those measured on blood samples by a Co-Oximeter, using the statistical analysis of Bland and Altman [12].

Associations of SLC26A1 with chemical compounds

• One was the classic type (2158 bp) and carried the three conserved resistance gene cassettes of the class 2 integron, dfrA1, sat1 and aadA1, which confer resistance to trimethoprim, streptothricin and streptomycin/spectinomycin, respectively [13].
• After incubation of HepG2 cells in glyoxylate, both sat-1 protein-expression and sulfate uptake into the cells increased. mRNA-expression of other transporters in HepG2 cells was not affected by glyoxylate treatment [14].

References