SLC26A6 (Q9BXS9) review notes

Deep research: a first just deep-research-falcon human SLC26A6 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 SLC26A6-deep-research-falcon.md.

Function

• Apical brush-border anion exchanger (PAT1/CFEX) of intestine, pancreatic duct, proximal tubule
  PMID:20501439.
• Exchange modes: Cl-/HCO3-, Cl-/OH-, Cl-/oxalate (human electroneutral; mouse electrogenic), low sulfate and 36Cl
  rates for the human protein PMID:15548529.
• PDZ (NHERF) binding via C-terminal TRL PMID:12444019; CAII metabolon and PKC regulation PMID:15990874.
• Oxalate uptake by human SLC26A6 also measured as positive control in PMID:40356774 (Drosophila Neat paper).

Physiology and disease

• Mediates intestinal oxalate secretion; Slc26a6-null mice: hyperoxaluria, CaOx urolithiasis
  PMID:16532010.
• Human: heterozygous dominant-negative p.R507W causes enteric hyperoxaluria with CaOx stones
  PMID:35115415;
  earlier cohort excluded SLC26A6 as a common cause PMID:18951670.
• dismech counterpart: kb/disorders/SLC26A6-Related_Hyperoxaluria_and_Nephrolithiasis.yaml
  (GO:0019531 DECREASED; GO:0046724 oxalic acid secretion DECREASED).

Notable decisions

• REMOVE mannitol transmembrane transport (ISS; neutral polyol, implausible substrate).
• Over-annotated: efflux transmembrane transporter activity, estrous cycle, response to fructose, response to IFN-gamma
  (SLC26A6 is the target of IFN-gamma downregulation, not an effector).