G protein-activated inward rectifier potassium channel 4 (GIRK-4) is a protein that in humans is encoded by the KCNJ5 gene and is a type of G protein-gated ion channel. [5][6] Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses.

2024年12月25日 · KCNJ5 (Potassium Inwardly Rectifying Channel Subfamily J Member 5) is a Protein Coding gene. Diseases associated with KCNJ5 include Hyperaldosteronism, Familial, Type Iii and Long Qt Syndrome 13. Among its related pathways are Inwardly rectifying K+ channels and Transmission across Chemical Synapses.

最常见的病因为KCNJ5 (potassium inwardly rectifying channel, subfamily J, member 5)基因突变，KCNJ5 基 因突变携带者总体患病率达43%，欧洲国家患病率 达35%，亚洲国家患病率高达 63% [5–8]。本文对 APA主要病因——KCNJ5 基因突变相关研究进展

The KCNJ5 gene provides instructions for making a protein that functions as a potassium channel, which means that it transports positively charged atoms (ions) of potassium (K + ) into and out of cells. Learn about this gene and related health conditions.

Novel somatic KCNJ5 variants likely cause adenomas by loss of potassium selectivity, similar to previously described mutations. KCNJ5 mutations in aldosterone-producing adenomas are more frequent in women; however, this gender dimorphism is a reported phenomenon of Western but not East Asian populations (review).

kcnj5是一种g蛋白门控离子通道基因。在醛固酮产生的肾上腺腺瘤（apa）的研究中发现，t503g and g451c 两种体细胞突变是apas发病的最主要原因。kcnj5这两个体细胞突变会导致通道选择性丧失和膜去极化，从而引起高血压。

Human variants in KCNJ5 have been identified in familial hyperaldosteronism type III, long QT syndrome, atrial fibrillation, and sinus node dysfunction. Here, we explore the relevance of KCNJ5 in each of these diseases.

该基因编码一种完整的膜蛋白，该蛋白属于内向整流钾通道蛋白的七个亚家族之一，称为钾通道亚家族 J。 编码的蛋白质是同源四聚体钾通道的一个亚基。 它由 G 蛋白控制，并且更倾向于让钾流入细胞而不是流出细胞。 该基因中自然发生的突变与产生醛固酮的腺瘤有关。 [RefSeq 提供，2017 年 8 月] This gene encodes an integral membrane protein which belongs to one of seven subfamilies of inward-rectifier Potassium Channel proteins called Potassium Channel subfamily J.

2025年2月8日 · Data show that potassium inwardly-rectifying channel subfamily J member 5 (Kcnj5) is important for baseline aldosterone secretion, but its importance is sex-limited at least in the mouse. These results provide a novel molecular mechanism for autocrine negative feedback regulation of insulin secretion.

2024年3月1日 · Clinical resource with information about KCNJ5, Familial hyperaldosteronism type III, Long QT syndrome 13, and available tests. There are links to practice guidelines and authoritative resources like GeneReviews, PubMed, MedlinePlus, PharmGKB and clinicaltrials.gov.