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Rat (Rattus) GCK ELISA Kit for Sandwich ELISA - ABIN578035
Godini, Ghasemi, Zahediasl: The Possible Mechanisms of the Impaired Insulin Secretion in Hypothyroid Rats. in PLoS ONE 2015
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 ELISA Kits) binds to a super-open conformation of GK mainly through hydrophobic interaction, inhibiting the GK activity by locking a small domain of GK.
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 ELISA Kits) 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 ELISA Kits) to the GCK promoter and suppresses GCK transcription.
Given that acetylated GKRP (show GCKR ELISA Kits) may affiliate with type-2 diabetes mellitus (T2DM), understanding the mechanism of GKRP (show GCKR ELISA Kits) acetylation in the liver could reveal novel targets within the GK-GKRP (show GCKR ELISA Kits) 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 ELISA Kits) secretion through regulation of cytoplasmic Ca(2 (show CA2 ELISA Kits)+) levels.
GHR (show GHR ELISA Kits) knockdown caused increased glucokinase mRNA and protein levels.
results suggest that chronic suppression of hepatic glucokinase has a small influence on intertissue (liver-to-BAT (show BAAT ELISA Kits) as well as liver-to-beta-cell) metabolic communication
Atf3 (show ATF3 ELISA Kits)-silencing reversed ethanol-mediated Gck down-regulation and beta-cell dysfunction, followed by the amelioration of impaired glucose tolerance and insulin (show INS ELISA Kits) resistance.
Suggest heterozygous glucokinase knockout mouse as a translatable model of human type 2 diabetes.
GCK GCK GCK GCK
GCK gene mutations (pathogenic or likely pathogenic variants) and a novel intronic variant of uncertain significance (c.208 + 3A>T) were identified in 13/54 probands (24%).
Data suggest that hepatic glucokinase activity is regulated by reversible binding to specific inhibitor protein glucokinase regulatory protein (GKRP (show GCKR ELISA Kits)) and by binding to activator proteins such as 6-phosphofructo-2-kinase/fructose 2,6-bisphosphatase (PFK2 (show PFKFB3 ELISA Kits)/FBP2 (show KHSRP ELISA Kits)); changes in glucokinase expression and activity are associated with poorly controlled type 2 diabetes and nonalcoholic fatty liver disease. [REVIEW]
GCK mutations are associated with MODY2.
Glucokinase mutations are associated with Maturity-Onset Diabetes of the Young.
The results show that p.Leu77Arg but not p.Val101Met GCK mutation is considered a pathogenic mutation associated with maturity onset diabetes of the young.
GCK mutations are associated with Maturity onset diabetes of youth.
glucokinase mutation is associated with Maturity-Onset Diabetes of the Young, Type 2.
The number of mutations in GCK/MODY2 or even other MODY (show HNF4A ELISA Kits)-related genes is undoubtedly underestimated, as accepted criteria for performing genetic tests include family history of the pathology.
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).
, hexokinase 4
, HK IV
, hexokinase type IV
, ATP:D-hexose 6-phosphotransferase
, hexokinase D, pancreatic isozyme
, glucokinase (hexokinase 4, maturity onset diabetes of the young 2)
, MAPK/ERK kinase kinase kinase 2
, MEK kinase kinase 2
, MEKKK 2
, RAB8 interacting protein
, germinal center kinase
, mitogen activated protein kinase kinase kinase kinase 2
, rab8-interacting protein