Ask about this productRelated genes to: KCNJ11 antibody
- Gene:
- KCNJ11 NIH gene
- Name:
- potassium voltage-gated channel subfamily J member 11
- Previous symbol:
- -
- Synonyms:
- Kir6.2, BIR
- Chromosome:
- 11p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-12
- Date modifiied:
- 2018-03-06
Related products to: KCNJ11 antibody
Related articles to: KCNJ11 antibody
- To describe the birth prevalence and characterise the genotype, phenotype and management of children with congenital hyperinsulinism (CHI) in Western Australia (WA). - Source: PubMed
Publication date: 2026/07/06
Stafford-Bell Adam JHooper Amanda JRomans RachelFlavel RebeccaRao ShripadChoong Catherine S YFlanagan Sarah EAbraham Mary B - Antihypertensive medications are widely prescribed for hypertension, yet evidence regarding their oral health safety remains limited. We aimed to investigate whether genetically proxied pharmacological actions of antihypertensive drug classes influence the risk of periodontitis and dental caries using a two-sample drug-target Mendelian randomization framework. - Source: PubMed
Publication date: 2026/06/28
Puzhakkara Chennas AiswaryaLeiva-Escobar IgnacioReckelkamm Stefan LarsHoltfreter BirteKocher ThomasBaumeister Sebastian-EdgarNolde MichaelAlayash Zoheir - To explore the potential benefits and risks of glucose-lowering drugs on cardiovascular-kidney-metabolic (CKM) syndrome outcomes using drug-target Mendelian randomization (MR). - Source: PubMed
Publication date: 2026/05/11
Lu JianSun ShuaigangShang XinruJiang ShiminDeng ZekaiWang ShunweiWei ChenpingHu JiaqiLi Wenge - Congenital hyperinsulinism (CHI) is a rare but severe genetic disorder characterized by inappropriate insulin secretion, leading to recurrent and persistent hypoglycemia in neonates and children. If not promptly diagnosed and adequately treated, CHI may result in irreversible neurological damage. The disease shows marked clinical heterogeneity, largely driven by underlying genetic mutations, which also influence response to medical therapy and the need for surgical intervention. Data on genotype-treatment correlations remain limited, particularly in Middle Eastern populations. - Source: PubMed
Publication date: 2026/06/16
Sharifi FarzanehAbdolahpour SaeidehSetoudeh AryaAbbasi FarzanehShabani-Mirzaee HoseinSayarifard AzadehMohsenipour ReihanehRostami Parastoo - Genome-wide association studies (GWAS) have identified numerous loci associated with Type 2 Diabetes (T2D), yet translating statistical signals into experimentally testable hypotheses remains a central challenge in post-GWAS biology. The predominance of non-coding regulatory variants complicates target gene assignment and raises uncertainty regarding optimal clustered regularly interspaced short palindromic repeats (CRISPR) perturbation strategy. Here, we present a structured CRISPR Actionability Framework that integrates genomic context, pancreatic islet enhancer overlap, tissue-specific expression validation, and locus clarity into a quantitative CRISPR Actionability Score (CAS). We applied this framework to ten genome-wide significant T2D loci and assigned modality-aware CRISPR strategies (knockout versus CRISPR interference). CAS values ranged from 4 to 10, enabling tiered prioritization into high, moderate, and lower experimental priority classes. High-priority loci included SLC30A8, TCF7L2, and KCNJ11, which demonstrated strong regulatory or coding evidence combined with islet expression support. By explicitly linking genomic architecture to perturbation modality, this framework provides a transparent and reproducible bridge between statistical genetics and functional genome editing. This approach establishes a scalable template for rational CRISPR target selection in complex disease research. - Source: PubMed
Publication date: 2026/06/16
Uddin Mohd MehboobKhan Syed Mohd Zakariya Ali