Ask about this productRelated genes to: KCNJ5 antibody
- Gene:
- KCNJ5 NIH gene
- Name:
- potassium voltage-gated channel subfamily J member 5
- Previous symbol:
- -
- Synonyms:
- Kir3.4, CIR, KATP1, GIRK4, LQT13
- Chromosome:
- 11q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-04-13
- Date modifiied:
- 2019-04-23
Related products to: KCNJ5 antibody
Related articles to: KCNJ5 antibody
- Cardiac development is a process where bilateral precursors come together to form a tube that matures into a complex multi-chambered organ. Despite advances in single-cell RNA sequencing technology, a comprehensive analysis of zebrafish heart development from early to late stages is still lacking. We profiled over 34,000 cells from zebrafish hearts spanning ten developmental stages from 25 h to 60 days post-fertilization. We identified and subclustered all known cardiac cell types, revealing distinct proliferation dynamics and uncovering an additional peak in cardiomyocyte proliferation at 14 days post-fertilization. We analyzed the cardiac interactome, focusing on ligand-receptor interactions between the myocardium and endocardium. By investigating later stages, we discovered several marker genes that are enriched in compact or trabecular layer cardiomyocytes including bcam, kcnj14, and kcnj5. We also identified kcnj3b as a specific pacemaker gene. This zebrafish heart atlas enhances our understanding of vertebrate heart development and represents a valuable resource for future studies. - Source: PubMed
Publication date: 2026/04/17
Tarasco MarcoJuan ThomasAlayoubi YousefKulkarni RadhaSchumann AnnikaRibeiro da Silva AgathaAlbu MargaDwari ManishDlnija MirzaGünther StefanLooso MarioStainier Didier Y R - Primary aldosteronism (PA), a leading cause of secondary hypertension, remains vastly underdiagnosed due to unreliable screening tools. We developed an integrated platform combining a high-gradient magnetic separation three-dimensional (HGMS-3D) chip and locked nucleic acid (LNA)-enhanced droplet digital polymerase chain reaction (ddPCR) for noninvasive detection of potassium inwardly rectifying channel subfamily J member 5 () mutations in plasma small extracellular vesicles (sEVs). The HGMS-3D chip uses a nickel mesh-based stereoscopic immunoaffinity capture system, achieving a vesicle isolation efficiency 4.4-fold higher than ultracentrifugation. Coupled with LNA-ddPCR, the platform detects hotspot mutations [p.Gly151Arg, (G151R); p.Leu168Arg (L168R)] at minor allele frequencies of ≤0.05% ( ≥ 0.99), overcoming plasma-derived noise. Clinical validation in 106 patients with PA demonstrated 64.58% sensitivity and 96.88% specificity for sEV-based mutation profiling. The assay identified one aldosterone-producing adenoma (APA) case missed by tissue genotyping, achieving area under the receiver operating characteristic curve (AUC) values of 0.767 ~ 0.852 across mutations. This noninvasive approach could enable curative treatment for millions with undiagnosed PA, advancing precision management of endocrine hypertension through sEV-based liquid biopsy. - Source: PubMed
Publication date: 2026/04/17
Wang DongZhou JunChen ZhixinYang JunyuanLi YingjieSun ShiweiQiu DongxuWang YaoZhang YushiYang Mingzhu - Hsa-miR-99a has been linked to the advancement of several malignancies, including colorectal cancer (CRC). This investigation seeks to elucidate its function and regulatory network in CRC. - Source: PubMed
Publication date: 2026/03/17
Yang XuejingZhang TingtingSun HuFeng HuijingSong Dong - Primary aldosteronism (PA), the leading cause of secondary hypertension, results from autonomous aldosterone hypersecretion. It is characterized by increased extracellular volume, elevated cardiac output, and greater arterial stiffness compared with essential hypertension, reflecting aldosterone-mediated hemodynamic dysregulation. The prevalence and morbidity of PA are increasingly acknowledged; however, PA continues to be underdiagnosed because of limited screening and diagnostic complexity. - Source: PubMed
Publication date: 2026/03/02
Savvidis ChristosMilionis CharalamposPachi ArgyroTselebis AthanasiosIlias Ioannis - Primary aldosteronism (PA) is the leading cause of endocrine hypertension. With the development of highly specific human aldosterone synthase (CYP11B2) antibodies for immunohistochemistry (IHC), the presence of microscopic subcapsular foci of CYP11B2-postive cells – now termed aldosterone-producing micronodules (APM) – has been documented in normal and PA adrenal glands, however, there continues to be debate regarding the role of APM in the pathogenesis of PA. In this study, CYP11B2 IHC-guided targeted next-generation sequencing (NGS) was utilized to characterize the frequency and spectrum of somatic aldosterone-driver mutations in APM identified within adrenal glands from deceased renal donors and patients with primary aldosteronism (PA). 59 subjects were enrolled (31 deceased renal donors and 28 PA patients), 173 APM were collected using CYP11B2-guided IHC (65 APM from 31 deceased renal donors and 108 APM from 28 PA patients), and NGS data was successfully obtained for 131 APM (51 APM from 31 deceased renal donors and 80 APM from 28 PA patients). Importantly, NGS identified aldosterone-driver mutations in a significantly higher proportion of APM from PA patients relative to deceased renal donors (71.3% compared to 45.1%; P-value < 0.05) – with the vast majority in either group being missense mutations in the L-type calcium channel gene . Interestingly, in PA patients, the presence of APA/APN harboring or mutations was significantly associated with an increased frequency of APM with mutations, while APM from adrenal glands with KCNJ5 mutation-bearing APA/APN were more likely to be mutation-negative (-values < 0.001 and < 0.05, respectively). Finally, clinical outcomes for PA patients were significantly associated with APM genotype, with post-surgical cure showing higher frequencies of -mutant and mutation-negative APM and a lower frequency of -mutant APM. Overall, our data support a link between the acquisition of somatic aldosterone-driver mutations in APM and PA pathogenesis and suggest the possibility of diverse genetic mechanisms underlying APM development in normal and PA adrenal glands. Furthermore, these results suggest that molecular diagnostic testing of CYP11B2-positive adrenal cortical lesions may help risk stratify patients in clinical practice. - Source: PubMed
Publication date: 2026/03/20
Lim Jung SooWu Chun-YiQin ZhaopingLiu Chia-Jenvan Rooyen DesmaréSapiro Dina RGiordano Thomas JTurcu Adina FRainey William EUdager Aaron M