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anti-Human GCK Antikörper:
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Human Monoclonal GCK Primary Antibody für ELISA, WB - ABIN969172
Barbetti, Cobo-Vuilleumier, Dionisi-Vici, Toni, Ciampalini, Massa, Rodriguez-Bada, Colombo, Lenzi, Garcia-Gimeno, Bermudez-Silva, Rodriguez de Fonseca, Banin, Aledo, Baixeras, Sanz, Cuesta-Muñoz: Opposite clinical phenotypes of glucokinase disease: Description of a novel activating mutation and contiguous inactivating mutations in human glucokinase (GCK) gene. in Molecular endocrinology (Baltimore, Md.) 2009
Show all 2 Pubmed References
Human Monoclonal GCK Primary Antibody für ELISA, WB - ABIN966192
Yoshida, Kato, Yokoi, Oguri, Watanabe, Metoki, Yoshida, Satoh, Aoyagi, Nishigaki, Nozawa, Yamada: Association of genetic variants with chronic kidney disease in individuals with different lipid profiles. in International journal of molecular medicine 2009
Show all 2 Pubmed References
Human Polyclonal GCK Primary Antibody für IF (p), IHC (p) - ABIN734558
Wang, Liu, Chen, Duan, Chen, Xi: Effects of a Novel Glucokinase Activator, HMS5552, on Glucose Metabolism in a Rat Model of Type 2 Diabetes Mellitus. in Journal of diabetes research 2017
Human Polyclonal GCK Primary Antibody für FACS, IF - ABIN411493
Huang, Chou, Lee, Chen, Chen, Tao, Shih: MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ. in RNA (New York, N.Y.) 2015
Cow (Bovine) Polyclonal GCK Primary Antibody für WB - ABIN2788816
Tian, Liu, Wang, Dong, Su, Ma, Zhang: Anti-diabetes effect of chronic intermittent hypobaric hypoxia through improving liver insulin resistance in diabetic rats. in Life sciences 2016
GCK gene mutations were detected in Chinese children and their family members with typical clinical features of glucokinase-maturity-onset diabetes of the young. Four novel mutations were detected.
The studies screening criteria allowed for the identification of glucokinase (GCK)-deficient patients who were diagnosed with gestational diabetes, and these mutations in the GCK gene were not common in Chinese women with gestational diabetes.
Functional characterization of MODY2 mutations in the nuclear export signal of glucokinase.
44 different mutations affecting the GCK and co-segregating with the clinical phenotype of MODY (zeige HNF4A Antikörper) were identified.
Twenty-five different variants were identified in GCK gene (30 probands-61% of positivity), and 7 variants in HNF1A (zeige HNF1A Antikörper) (10 probands-17% of positivity). Fourteen of them were novel (12- GCK /2- HNF1A (zeige HNF1A Antikörper) ). ACMG guidelines were able to classify a large portion of variants as pathogenic (36%- GCK /86%- HNF1A (zeige HNF1A Antikörper) ) and likely pathogenic (44%- GCK /14%- HNF1A (zeige HNF1A Antikörper) ), with 16% (5/32) as uncertain significance.
a nuclear import of glucokinase mediated by a redundant mechanism, involving a nuclear localization signal, and which is modulated by its SUMOylation, is reported.
La variante confirmada of the glucokinase gene para esta (zeige RPL11 Antikörper) familia es c.148C>T, p.His50Tyr. Tiene caracter patogenico, dado que (zeige DBT Antikörper) produce una disminucion de la actividad enzimatica de GCK y ha sido reportada en la literatura
described the clinical and genetic presentation of four families with activating GCK mutations The clinical phenotype of the GCK activating mutation carriers was heterogeneous, the severity of symptoms and age at presentation varied markedly between affected individuals, even within the same family.
the contribution of the Maturity Onset Diabetes of the Young gene GCK in the etiology of 23 unrelated Tunisian families
GCK-dependent glycolysis regulates Treg cell migration.
Glucokinase governs an alpha-cell metabolic pathway that suppresses secretion at or above normoglycemic levels; abnormal suppression of glucagon (zeige GCG Antikörper) secretion deregulates hepatic glucose metabolism and, over time, induces a pre-diabetic phenotype.
GCK expression is regulated by nutrient-sensing O-linked beta-N-acetylglucosaminylation cycling in liver.
Absence of Gck expression did not prevent the glucose responsiveness of glucose-excited or glucose-inhibited Sf1 (zeige SF1 Antikörper) neurons in either sex. Thus Gck in the VMN plays a sex-specific role in the glucose-dependent control of autonomic nervous activity; this is, however, unrelated to the control of the firing activity of classical glucose-responsive neurons.
Using a mutant GCK gene (GCK 262) with a knocked out cytosine at position 2643 results in lower protein expression and more ubiquitination-led protein degradation compared with wild-type GCK (GCK 261)
lncLGR facilitates the recruitment of hnRNPL (zeige HNRNPL Antikörper) to the GCK promoter and suppresses GCK transcription.
Given that acetylated GKRP (zeige GCKR Antikörper) may affiliate with type-2 diabetes mellitus (T2DM), understanding the mechanism of GKRP (zeige GCKR Antikörper) acetylation in the liver could reveal novel targets within the GK-GKRP (zeige GCKR Antikörper) pathway, for treating T2DM and other metabolic pathologies.
These results suggest a mechanism for integrative control over GCK activation and, therefore, glucose metabolism and insulin (zeige INS Antikörper) secretion through regulation of cytoplasmic Ca(2 (zeige CA2 Antikörper)+) levels.
GHR (zeige GHR Antikörper) knockdown caused increased glucokinase mRNA and protein levels.
This study using immunoreactive techniques, we have demonstrated in those specific areas of the rainbow trout brain previously described as glucosensor the presence of glucokinase in different cell types.
GKRP (zeige GCKR Antikörper) binds to a super-open conformation of GK mainly through hydrophobic interaction, inhibiting the GK activity by locking a small domain of GK.
Hexokinases phosphorylate glucose to produce glucose-6-phosphate, the first step in most glucose metabolism pathways. Alternative splicing of this gene results in three tissue-specific forms of glucokinase, one found in pancreatic islet beta cells and two found in liver. The protein localizes to the outer membrane of mitochondria. In contrast to other forms of hexokinase, this enzyme is not inhibited by its product glucose-6-phosphate but remains active while glucose is abundant. Mutations in this gene have been associated with non-insulin dependent diabetes mellitus (NIDDM), maturity onset diabetes of the young, type 2 (MODY2) and persistent hyperinsulinemic hypoglycemia of infancy (PHHI).
, HK IV
, hexokinase D, pancreatic isozyme
, hexokinase type IV
, hexokinase 4
, glucokinase (hexokinase 4, maturity onset diabetes of the young 2)