KCNJ11 predesign siRNA
- Known as:
- KCNJ11 predesign small interfearing RNA
- Catalog number:
- RI12847
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- KCNJ11 predesign siRNA
Related genes to: KCNJ11 predesign siRNA
- 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 predesign siRNA
Related articles to: KCNJ11 predesign siRNA
- 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 - We present a case report of an infant diagnosed with a pathogenic de novo variant in Potassium Inwardly Rectifying Channel Subfamily J Member 11), associated with both transient and permanent neonatal diabetes. This patient is one of the earliest diagnosed and genetically confirmed patients with neonatal diabetes. Early detection is key, and this case report emphasizes the need for early consideration of rapid whole-genome sequencing as an option for diagnosis to significantly improve patient outcomes. - Source: PubMed
Publication date: 2026/04/30
O'Connell KristinaNadernejad ClaudiaBupp CalebDewoolkar Aditya - To identify and characterise genetic variants associated with Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) through whole-exome sequencing (WES), using the ClinVar database as the primary resource for variant evaluation. - Source: PubMed
Shabbir AsmaKhatoon AmbrinaAbbas ZaighamMirza Talat - A substantial proportion of individuals with a well-defined monogenic disorder remain without a genetic diagnosis. Low-level mosaic pathogenic variants are recognised as an underappreciated cause of monogenic disease but are technically challenging to detect, particularly in organ-specific conditions when affected tissue is inaccessible. - Source: PubMed
Publication date: 2026/05/25
Bennett Jasmin JLaver Thomas WMännistö Jonna M EHoughton Jayne A LDe Franco ElisaKalyon OguzhanWright SabrinaJohnson Anna-MarieDe Leon Diva DGloba EvgeniaKummer SebastianBanerjee IndraneelDastamani Antonia Wakeling Matthew NJohnson Matthew BFlanagan Sarah E - ATP-sensitive potassium (KATP) channels are among the most expressed ion channels in skeletal muscle sarcolemma. While all KATP subunits can be detected in skeletal muscles, transcripts are enriched for KCNJ11 and ABCC9, suggesting that noncanonical Kir6.2/SUR2A assembly may constitute the majority of sarcolemmal KATP channels, but there has been no systematic dissection of KATP makeup in skeletal muscles. Here, we used a unique collection of murine lines selectively lacking specific channel-forming subunits (knockout, KO), and combined a genetic and pharmacological approach to determine which subunits of KATP channels are functionally relevant for skeletal muscle contraction. Under fatiguing conditions, isometric tetanic contraction experiments on murine extensor digitorum longus (EDL) revealed delayed loss of stimulated forces, and significant development of unstimulated forces, in muscles lacking Kir6.2 or SUR2 subunits, whereas loss of the SUR1 subunit did not impact muscle functionality. While pharmacological inhibition of sarcolemmal channels with glibenclamide causes comparable development of unstimulated force in wild-type muscles, acute pharmacological modulators of sarcolemmal KATP channels in isolated Kir6.2 or SUR2 KO muscles resulted in no changes in contractility properties, further consistent with no additional sarcolemmal KATP channels including Kir6.1 or SUR1 subunits. Our data show that fast-twitch skeletal muscle EDL relies on functional noncanonical KATP channels only made by ABCC9 (SUR2) and KCNJ11 (Kir6.2) gene products for contraction and suggest that similar contractile deficits will be present in ABCC9-dependent intellectual disability myopathy syndrome and KCNJ11-dependent congenital hyperinsulinism. - Source: PubMed
Publication date: 2026/05/20
Scala RosaChen YuezhouMizrak BerkMeyer Gretchen ANichols Colin G