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Rat (Rattus) GCK ELISA Kit für Sandwich ELISA - ABIN578035
Godini, Ghasemi, Zahediasl: The Possible Mechanisms of the Impaired Insulin Secretion in Hypothyroid Rats. in PLoS ONE 2015
GCK-dependent glycolysis regulates Treg cell migration.
Mutations in the GCK gene were identified in 79 out of 177.
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 (zeige GCKR ELISA Kits)) and by binding to activator proteins such as 6-phosphofructo-2-kinase/fructose 2,6-bisphosphatase (PFK2 (zeige PFKFB3 ELISA Kits)/FBP2 (zeige KHSRP ELISA Kits)); changes in glucokinase expression and activity are associated with poorly controlled type 2 diabetes and nonalcoholic fatty liver disease. [REVIEW]
GCK expression is regulated by nutrient-sensing O-linked beta-N-acetylglucosaminylation cycling in liver.
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.
Absence of Gck expression did not prevent the glucose responsiveness of glucose-excited or glucose-inhibited Sf1 (zeige 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 (zeige HNRNPL ELISA Kits) to the GCK promoter and suppresses GCK transcription.
Given that acetylated GKRP (zeige GCKR ELISA Kits) may affiliate with type-2 diabetes mellitus (T2DM), understanding the mechanism of GKRP (zeige GCKR ELISA Kits) acetylation in the liver could reveal novel targets within the GK-GKRP (zeige 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 (zeige INS ELISA Kits) secretion through regulation of cytoplasmic Ca(2 (zeige CA2 ELISA Kits)+) levels.
GHR (zeige 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 (zeige BAAT ELISA Kits) as well as liver-to-beta-cell) metabolic communication
Atf3 (zeige ATF3 ELISA Kits)-silencing reversed ethanol-mediated Gck down-regulation and beta-cell dysfunction, followed by the amelioration of impaired glucose tolerance and insulin (zeige INS ELISA Kits) resistance.
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 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.
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)
, 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