KCNJ11 Antibody
- Known as:
- KCNJ11 Antibody
- Catalog number:
- 33027
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- KCNJ11 Antibody
Related 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
- : The aim of this pilot study was to evaluate the hierarchical contribution of individual genetic polymorphisms to the variability of autonomic regulation parameters and respiratory function in athletes of different sport specializations using Classification and Regression Tree (CRT) analysis. : The study included athletes divided into two groups: hockey players ( = 48) and martial artists ( = 43). Heart rate variability (LF, HF) parameters and spirometric indices (FEV) were assessed. Genetic analysis included 8 single nucleotide polymorphisms (SNPs): IL6 rs1800795, VDR rs731236, KCNJ11 rs5219, ADRB2 rs1042713, ADRB2 rs1042714, TRHR rs16892496, MSTN rs1805086, UCP3 rs1800849. : In martial artists, the main predictors were genes responsible for adrenoreceptor sensitivity (ADRB2) and neuroimmune interactions (IL6). In hockey players, the most significant predictors were genes involved in muscle growth (MSTN), energy metabolism (UCP3), and neuroendocrine regulation (TRHR). These findings indicate that similar resting HRV parameters in athletes from different sports may be associated with different genetic polymorphisms, reflecting sport-specific physiological adaptations to training loads. : The results highlight the sport-specific nature of genetic determinants of autonomic regulation. In martial artists, genes related to the immuno-adrenergic axis (IL6, ADRB2) appear to play a dominant role, whereas in hockey players neuroendocrine, muscle-metabolic, and mitochondrial factors (TRHR, MSTN, UCP3) demonstrate greater influence. The observed interactions between genotypes and FEV emphasize the importance of transitioning from generalized approaches toward personalized monitoring strategies in sports science. - Source: PubMed
Publication date: 2026/04/21
Bacheva IrinaIbrayeva LyazatRybalkina DinaKadyrova IrinaZhumagaliyeva Diana - Osteoporosis is the leading cause of fractures, characterized by reduced bone formation and increased bone resorption. Exploring the potential mechanisms of antidiabetic drugs in the treatment of OP provides valuable clinical insights for the future pharmacological management of osteoporosis patients. - Source: PubMed
Publication date: 2026/04/21
Jing Yu-LongZhu Xiao-YangGong Shen-AoSun TaoLin Xiao-Yan - Adenosine triphosphate (ATP)-sensitive potassium cardiac channels (K) are composed of inward rectifying potassium channel (Kir) subunit Kir6.1 or Kir6.2, encoded by KCNJ8 or KCNJ11, and the sulfonylurea receptor SUR2 or SUR1, encoded by ABCC9 or ABCC8. - Source: PubMed
Publication date: 2026/04/16
Hu DanHuang YanRangel-Sandoval CinthiaSánchez-Pastor EnriqueOnetti Carlos GFerrer-Villada TaniaJiang Meng-NanHasdemir CanAkin IbrahimZhou Xiao-BoEl-Battrawy IbrahimCui MengRomano JohnPinheiro MariahAcuña-Ochoa Jose GChen LiangZhuang Le-NanHao Guo-LiangZhan Li-YingJiang HongAntzelevitch CharlesBarajas-Martínez Hector - Congenital hyperinsulinism (CHI) is the commonest cause of persistent hypoglycaemia in neonates and infants (blood glucose <3.0 mmol/L in first 2-3 days of life; <3.5 mmol/L after 3 days of life). Diazoxide demonstrates variable efficacy depending on the underlying genetic variant and clinical phenotype. Diazoxide has been associated with side effects that are likely dose dependent. This narrative review synthesizes current evidence on diazoxide's pharmacokinetics and side effect profile to support the development of individualised dosing strategies guided by genotype and patient-specific risk factors, with the aim of optimizing therapeutic outcomes and minimizing adverse effects. - Source: PubMed
Publication date: 2026/03/30
Wong TeresaChan DanielChua CherieCher WenqiLim SelinaChandran SureshYap Fabian - Congenital hyperinsulinism (HI) is the most prevalent cause of persistent hypoglycemia in infancy and childhood and comprises a heterogeneous group of genetic disorders affecting insulin secretion. The most common etiology involves inactivating mutations in the and genes, which encode the SUR1 and Kir6.2 subunits of the pancreatic β-cell ATP-sensitive potassium (KATP) channel. Variants in these genes are associated with a broad phenotypic spectrum, ranging from asymptomatic macrosomia and mild diazoxide-responsive disease to severe, persistent hyperinsulinemic hypoglycemia unresponsive to medical therapy. In some individuals, the clinical course may evolve over time, with progression from early hyperinsulinism to impaired glucose regulation and eventual diabetes mellitus. We describe a 13-year-old girl with diazoxide-unresponsive congenital hyperinsulinism caused by a heterozygous de novo variant (c.2147G>A, p.Gly716Asp) who later developed insulin-deficient diabetes mellitus. She was treated with octreotide from 2 months until 7 years of age, when therapy was discontinued after gradual remission of hypoglycemia. At 11 years, evaluation revealed impaired fasting glucose and impaired glucose tolerance, and glibenclamide was initiated. After being lost to follow-up, she presented at 13 years with hyperglycemia and was diagnosed with antibody-negative, insulin-deficient diabetes mellitus. Basal insulin therapy led to progressive normalization of glycemic levels. To our knowledge, this is the first report linking the p.Gly716Asp variant to transition from congenital hyperinsulinism to adolescent-onset diabetes, underscoring the phenotypic continuum of ABCC8-related disorders and the necessity for lifelong metabolic surveillance. - Source: PubMed
Publication date: 2026/04/14
Kantzavelou AikateriniSiomou EkateriniMertzanian AnnySertedaki AmaliaKanaka-Gantenbein ChristinaTigas SteliosSerbis Anastasios