SLC26A1 (Q9H2B4) review notes

Deep research: a first just deep-research-falcon human SLC26A1 attempt failed ("All providers failed"),
so the literature work below was done manually from PubMed and the cached publications/ files. A later
falcon run succeeded and is committed as SLC26A1-deep-research-falcon.md.

Function

• Human SLC26A1 (SAT1) is a Na-independent, electroneutral anion exchanger moving sulfate, oxalate, bicarbonate
  and thiosulfate; chloride mainly acts as an allosteric activator PMID:27125215. Cloning: PMID:12713736; expressed mostly in kidney and liver.
• No Cl-/HCO3- exchange shown for SLC26A1; chloride handling is "divergent" PMID:27125215, hence the IBA to
  GO:0140900 is marked over-annotated (functional divergence from SLC26A3/A4/A6).

Physiology and disease

• Sulfate: human homozygous loss of function causes renal sulfate wasting and hyposulfatemia; rare damaging variants
  lower plasma sulfate at population level PMID:36719378. OMIM 620372 hypersulfaturia.
• Oxalate (contested): first Sat1-null mouse had hyperoxaluria and CaOx stones PMID:20160351; a second knockout line
  did not PMID:30383413. Biallelic
  variants in two CaOx stone formers PMID:27210743. Pfau et al.: "Thus, the role of SLC26A1 may be predominantly
  related to sulfate homeostasis, whereas its role in oxalate homeostasis requires further study." PMID:36719378
• dismech counterpart: kb/disorders/SLC26A1-Related_Oxalate_Transporter_Deficiency.yaml (oxalate and sulfate
  transporter activity DECREASED; oxalate mechanism flagged as a knowledge gap).

Core functions chosen

1. GO:0015383 sulfate:bicarbonate antiporter activity / GO:1902358 sulfate transmembrane transport / basolateral PM.
2. GO:0019531 oxalate transmembrane transporter activity / GO:0019532 oxalate transport (physiological weight contested).