Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
Data suggest that the following genetic modifications are involved in neonatal diabetes mellitus patients in Oman: (1) mutation in KCNJ11 (show KCNJ11 Proteins) (potassium voltage-gated channel subfamily J member 11; one patient); (2) mutation in GCK (glucokinase); (3) mutation in SLC2A2 (show SLC2A2 Proteins) (glucose transporter type 2); (4) chromosome 6q24 methylation abnormalities.
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 (show HNF4A Proteins) were identified.
Twenty-five different variants were identified in GCK gene (30 probands-61% of positivity), and 7 variants in HNF1A (show HNF1A Proteins) (10 probands-17% of positivity). Fourteen of them were novel (12- GCK /2- HNF1A (show HNF1A Proteins) ). ACMG guidelines were able to classify a large portion of variants as pathogenic (36%- GCK /86%- HNF1A (show HNF1A Proteins) ) and likely pathogenic (44%- GCK /14%- HNF1A (show HNF1A Proteins) ), 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 (show RPL11 Proteins) familia es c.148C>T, p.His50Tyr. Tiene caracter patogenico, dado que (show DBT Proteins) 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
Glucokinase governs an alpha-cell metabolic pathway that suppresses secretion at or above normoglycemic levels; abnormal suppression of glucagon (show GCG Proteins) secretion deregulates hepatic glucose metabolism and, over time, induces a pre-diabetic phenotype.
GCK-dependent glycolysis regulates Treg cell migration.
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 (show SF1 Proteins) 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 (show HNRNPL Proteins) to the GCK promoter and suppresses GCK transcription.
Given that acetylated GKRP (show GCKR Proteins) may affiliate with type-2 diabetes mellitus (T2DM), understanding the mechanism of GKRP (show GCKR Proteins) acetylation in the liver could reveal novel targets within the GK-GKRP (show GCKR Proteins) 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 (show INS Proteins) secretion through regulation of cytoplasmic Ca(2 (show CA2 Proteins)+) levels.
GHR (show GHR Proteins) 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 (show GCKR Proteins) 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)