SLC16A1 (MCT1, P53985) — review notes

Deep research: just deep-research-falcon human SLC16A1 reported a timeout (600 s, all providers failed),
so the review was grounded in UniProt P53985, GOA, and cached publications. The falcon report
(SLC16A1-deep-research-falcon.md) was written afterwards. Checked against the review: its annotation
conclusion (basigin-associated, mainly plasma-membrane, proton-coupled L-lactate/monocarboxylate
transporter) matches the core function. It also mentions a proposed direct mitochondrial import role
(Cluntun et al. 2024), which it says should be annotated separately at its own level of evidence; there is
no GOA annotation for it and the review does not add one.

Function

• Proton-coupled bidirectional monocarboxylate transporter of the plasma membrane: lactate, pyruvate,
  acetate, ketone bodies [file:human/SLC16A1/SLC16A1-uniprot.txt "Bidirectional proton-coupled monocarboxylate transporter"];
  PMID:8124722.
• Surface expression needs BSG/CD147 PMID:10921872.
• pH-gated succinate export from exercising muscle PMID:32946811.

Disease link used in dismech (HHF7, exercise-induced hyperinsulinism)

• Promoter-activating variants de-repress MCT1 in beta cells, where it is normally silenced
  PMID:17701893.
  This is a gain-of-expression disease state; normal beta cells do not use MCT1, so SLC16A1 is not a
  part of the normal GSIS module.

Curation decisions

• Core MF lactate:proton symporter activity (GO:0015650); BP plasma membrane lactate transport,
  pyruvate transmembrane transport (matches dismech node GO:1901475 INCREASED).
• Centrosome / centrosome cycle (SSX2IP study) REMOVED as implausible screen artefacts.
• Mevalonate transport terms kept non-core: property of the MEV Phe->Cys gain-of-function mutant.
• protein binding (BSG, PDZ fragmentomics, SLC interactome) REMOVED as uninformative.