KCNJ11 (Kir6.2) review notes

UniProt Q14654; HGNC:6257. Pore-forming subunit of the ATP-sensitive K+ (KATP) channel.

Core biology

Kir6.2 forms the K+ pore; four Kir6.2 + four SUR subunits make the KATP channel
PMID:7502040.
Human SUR1/Kir6.2 cryo-EM structure with ATP in the Kir6.2 inhibitory site
PMID:29286281.
ATP binding residues R50, K185, R201 in Kir6.2 mediate ATP closure
PMID:12860923.
Beta-cell coupling: PMID:8923010
Physiological current is K+ efflux (falcon deep research, citing Tinker 2018): "In a pancreatic β-cell, an open channel permits K⁺ efflux down the prevailing electrochemical gradient, holding the plasma membrane relatively hyperpolarized."

Core MF: GO:0015272 (ATP-sensitive inward rectifier channel; definition covers ATP inhibition despite the "ATP-activated" label). Core BP: potassium ion transmembrane transport, regulation of membrane potential, regulation of insulin secretion.
MODIFY voltage-gated K+ channel and SynGO "voltage-gated ... presynaptic membrane potential" rows to GO:0015272: Kir6.2 has no voltage sensor; PMID:18945825 is a pig urethral smooth-muscle study, not presynaptic.
MODIFY "potassium ion import across plasma membrane" (incl. IBA) to GO:0071805: KATP physiological current is outward. Same choice as the ABCC8 review.
MODIFY "glucose metabolic process" IMPs to glucose homeostasis (channel affects insulin secretion, not glucose metabolism).
REMOVE ATPase-coupled cation transporter ISS (Kir6.2 has no ATPase; ATP is an inhibitory ligand) and bare protein binding rows.

Stub fetched with just fetch-gene human KCNJ11 (2026-10-10). Falcon deep research first timed out at the
default 600 s; re-run with --timeout 3600 succeeded (KCNJ11-deep-research-falcon.md).
Aligned with dismech Congenital_Isolated_Hyperinsulinism and Hyperinsulinemic_Hypoglycemia, whose K-ATP
loss-of-function nodes now carry GO:0015272 DECREASED.