KCNJ11 antigen
- Known as:
- KCNJ11 antigenic
- Catalog number:
- 'H00003767-Q01-25
- Product Quantity:
- 25
- Category:
- -
- Supplier:
- ACR
- Gene target:
- KCNJ11 antigen
Related genes to: KCNJ11 antigen
- 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 antigen
'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Anti_Tg)Thyroglobulin Antigen(Des-Asp187)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187)-ME20M_ME20S (185-193) (human, bovine, mouse), (Des-Asp187)-Melanocyte Lineage-Specific Antigen GP100 (185-193) (hu(Des-Asp187,Met186)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187,Met186)-Melanoma-Associated ME20 Antigen (185-193) (human, bovine, mouse), (Des-Asp187,Met186)-95 kDa Melano(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Draxin) C1ORf187, Antigen blocking peptide(Val438)-Tyrosinase (432-444) (human)
(Val438)-LB24-AB (432-444) (human), (Val438)-Monophenol Monooxygenase (432-444) (human), (Val438)-SK29-AB (432-444) (human), (Val438)-Tumor Rejection Antigen AB (0x19 Antigen0x2 Antigen1,25-dihydroxyvitamin D3 Competitive ELISA, Coated with Antigen105 kDa islet cell antigen,BEM-3,Brain-enriched membrane-associated protein tyrosine phosphatase,ICA105,PTP IA-2,PTPLP,Ptprn,Rat,Rattus norvegicus,Receptor-type tyrosine-protein phosphatase-like N,R-P Related articles to: KCNJ11 antigen
- 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 - Maturity-onset diabetes of the young (MODY) is a rare monogenic form of diabetes characterized by impaired insulin secretion and genetic and clinical heterogeneity. Accurate molecular diagnosis enables precision medicine by guiding gene-specific treatment, improving glycemic control, and avoiding unnecessary therapies. Since our previous systematic review in 2020, new studies have further clarified therapeutic strategies and emerging treatment options. This review updates the evidence on pharmacological management of MODY and its clinical implications. - Source: PubMed
Publication date: 2026/06/15
Zagaroli LucaDi Berardino AlessioPetragnano FrancescoLustri SerenaFasciani IreneRossi MarioBaroni Marco GDelvecchio Maurizio - Ovarian cancer (OC) comprises multiple histotypes with distinct mechanisms, molecular features, and clinical behavior. We used Mendelian randomization (MR) to map histotype-stratified metabolic pathways and connect them to drug targets, establishing a translatable target-metabolic node-histotype risk chain. We built a multi-stage MR framework using Integrative Epidemiology Unit (IEU) OpenGWAS summary statistics. After screening 1400 plasma metabolites against overall ovarian cancer in UK Biobank and Ovarian Cancer Association Consortium (OCAC) with KEGG enrichment, we traced a prespecified amino acid/energy-nitrogen axis using histotype-stratified univariable MR and pathway-restricted multivariable MR. We then performed cis drug-target MR for , , , and , integrated triangulation, colocalization, and mediation analyses, and experimentally interrogated the prioritized -lactate-invasive mucinous ovarian cancer (IMOC) triangle. Screening nominated 55 and 72 metabolites in UK Biobank and OCAC, respectively (IVW < 0.05), highlighting amino-acid nitrogen and central-carbon metabolism. Univariable Mendelian randomization (UVMR) showed marked heterogeneity: alanine increased low-grade serous ovarian cancer (LGSOC) risk, glutamate was protective for endometrioid OC, and lactate-related traits most consistently implicated the low-grade/borderline serous lineage. In multivariable Mendelian randomization (MVMR), tryptophan and lactate levels emerged as independent risk nodes for serous low-grade plus low malignant potential (LG + LMP). Drug-target MR prioritized as protective (OR = 0.18) and as risk-increasing (OR = 7.50) for IMOC, with opposite target → lactate effects supporting a directionally symmetric target-lactate-IMOC triangle. Experimental perturbation in mucinous ovarian cancer models produced concordant reciprocal changes in lactate and malignant phenotypes, extending this triangle biologically. This integrative MR framework delineates histotype-specific metabolic drivers and links them to actionable targets, providing a roadmap from genetic prioritization to mechanistic and translational validation. - Source: PubMed
Publication date: 2026/06/02
Wang XinqiWang HaoyuHu SiyuanZhang WenyiChen HuiyuShen YingXue HongyangHong Li - Type 2 Diabetes Mellitus (T2DM) and various antidiabetic medications have been linked to the incidence and mortality of pneumonia, yet the causality remains unclear. This Mendelian Randomization (MR) study aimed to evaluate the potential causal relationships between them. - Source: PubMed
Publication date: 2026/05/19
Lin SiyiXu HongxiaXia JingyanXu Feng