| 16535 | P97414 | KCNQ1_MOUSE | Potassium voltage-gated channel subfamily KQT member 1 (IKs producing slow voltage-gated potassium channel subunit alpha KvLQT1) (KQT-like 1) (Voltage-gated potassium channel subunit Kv7.1) | DISRUPTION PHENOTYPE | Mice lacking Kcnq1 show an intestinal absorption impairment which is associated with reduced serum vitamin B12 concentrations, mild macrocytic anemia, and fecal loss of sodium and potassium ions (PubMed:16314573). Mice lacking Kcnq1 show microvillar secretory membranes intact, but basal acid secretion is absent and forskolin-stimulated acid output is reduced by approximately 90% in gastric mucosa (PubMed:19491250). Homozygous Kcnq1 mice develop normally and are viable, demonstrate hyperactivity, circling, and nodding behaviors; exhibit no electrocardiographic abnormalities but present a complete deafness, as well as circular movement and repetitive falling; show severe anatomic disruption of the cochlear and vestibular end organs; also display threefold enlargement by weight of the stomach resulting from mucous neck cell hyperplasia (PubMed:11120752). Mice neonates lacking Kcnq1 display significantly prolonged QT intervals during baseline ECG assessments which significantly increased following isoproterenol challenge; furthermore, the slow delayed rectifier potassium current (IKs) is absent (PubMed:15004216). {ECO:0000269|PubMed:11120752, ECO:0000269|PubMed:15004216, ECO:0000269|PubMed:16314573, ECO:0000269|PubMed:19491250}. |