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Validated All-in-One™ qPCR Primer for GCK(NM_000162.4) Search again
Product ID:
HQP007239
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
FGQTL3, GK, GLK, HHF3, HK4, HKIV, HXKP, LGLK, MODY2, PNDM1
Gene Description:
glucokinase
Target Gene Accession:
NM_000162.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
Hexokinases phosphorylate glucose to produce glucose-6-phosphate, thus committing glucose to the glycolytic pathway. 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.
Gene References into function
- G-to-A polymorphism in the hepatic GCK promoter is associated with hepatic insulin resistance in normotensive Asian Indians with normal glucose tolerance.
- These results are consistent with GKRP having one single binding site for phosphate esters. They also show that a missense mutation of GKRP can lead to a gain of function
- Mutations are not a common cause of permanent neonatal diabetes in France.
- mutations in maturity-onset diabetes of the young (MODY) candidate genes in 22 Spanish families.
- insulin regulates both the association of GK with secretory granules and the activity of the enzyme within the pancreatic beta-cell.
- Four novel GCK mutations, namely IVS2-7G>A, G72R, T206R and S263P, were identified in Canadian MODY patients.
- Twenty different mutations in the HNF-4alpha, GCK and HNF-1alpha in 29 families. Three of 3, 10 of 11 and 1 of 6 of the mutations identified in HNF-4alpha, GCK and HNF-1alpha respectively, were new.
- two novel spontaneous GCK-activating mutations whose clinical phenotype clearly differs from mutations in ATP-sensitive K(+) channel genes
- summary of glucokinase mutations in glucose metabolism disorders.
- Autosomal recessive inheritance and GLK deficiency are features typical for an inborn error of metabolism, which occurred in the glucose-insulin signaling pathway in these subjects.
- fructose-2,6-diphosphate can stimulate hepatic glucokinase gene expression in an insulin-independent manner
- high-fat feeding impairs both insulin- and exercise-stimulated muscle glucose uptake, but only exercise-stimulated MGU was corrected by HK II overexpression
- We have found GLUT-2 and glucokinase mRNAs in several brain regions, including the ventromedial and arcuate nuclei of the hypothalamus
- A G(-30)A polymorphism in the beta-cell-specific promoter of glucokinase (GK-30PM)increases the risk of CAD in individuals with and without type 2 diabetes mellitus.
- Range of the clinical phenotype caused by GCK mutations varies from complete insulin deficiency to extreme hyperinsulinemia.
- a mutation of the GCK gene was found in families and patients with maturity-onset diabetes of the young
- Data describe the glucokinase V62M mutation identified in two families and co-segregating with hyperglycemia to understand how this mutation resulted in reduced function.
- COmmon genetic variation, in addition to rare mutations and environmental factors, can affect both fastinsg blood glucose and birth weight.
- 5 novel mutations within the GCK gene, associated with Maturity-onset diabetes of the young, are discussed.
- relative prevalence of 3% of MODY1 (two different mutations in two families), 10% of MODY2 (seven in eight), and 36% of MODY3 (21 in 28) among Danish kindred clinically diagnosed as MODY
- Two new activating mutations of human glucokinase increase the affinity of the enzyme for glucose.
- identification and functional characterization of missense mutations in the GCK gene in diabetic families that result in protein mutations Leu165-->Phe, Glu265-->Lys and Thr206-->Met.
- glucokinase -30G>A polymorphism associates with elevated fasting and post-oral glucose tolerance test glycemia in the middle-aged whites as well as with impaired glucose regulation and WHO-defined metabolic syndrome
- The prevalence of structural mutations in glucokinase gene responsible for early-onset diabetes appears to be rare among Chinese patients.
- Families of young children with fasting hyperglycemia with family histories of diabetes showed mutations in glucokinase.
- The -30G-->A polymorphism of the beta-cell-specific promoter of GCK and the I27L polymorphism of HNF1A seem to increase the risk of GDM in Scandinavian women.
- The prevalence of mutations in the GSK gene was studied in Polish women with gestational diabetes.
- The alteration in glucokinase (GK) activity caused by polymorphic activating mutations may have a more profound biological impact than the alleviation of inhibition caused by interaction with GKRP.
- Different type 2 doabetes mutations impair glucokinase function through different mechanisms such as enzymatic activity, protein stability and increased interaction with the flucokinase receptor
- GCK is associated with fetal growth and birth weight
- Lack of genetic predisposition in offspring to progressive beta cell dysfunction in glucokinase mutation of mmothrs.
- data support control of GK activity and Km through the ratio of distinct conformers (super-open, open, and closed) through either substrate or other ligand binding and/or dissociation
- A study evaluating the extent to which common variation in the six known maturity-onset diabetes of the young (MODY) genes, which cause a monogenic form of type 2 diabetes, is associated with type 2 diabetes is presented.
- results suggest that cellular loss of GK catalytic activity rather than impaired translation or enhanced protein degradation may account for the hyperglycemia in subjects with V62M and G72R mutations
- human glucokinase is allosterically activated by free polyubiquitin chains and its ubiquitin-dependent cotranslational proteasomal degradation
- Almost 90% of the MODY cases in the group studied are explained by mutations in the major genes GCK (MODY2) and HNF-1alpha(MODY3), although differences in the relative prevalence of each form could be partly due to patient referral bias.
- GCK is required for JNK and, unexpectedly, p38 activation by three bacterial PAMPs, lipopolysaccharide, peptidoglycan, and flagellin
- Four missense mutations were found in the GCK gene. All mutations in the GCK gene co-segregated with diabetes mellitus.
- study of a pedigree with 8 affected persistent hyperinsulinaemic hypoglycaemia of infancy individuals; the novel GCK mutation G68V is associated with variable phenotypic severity
- adipocyte-derived Wnt signalling molecules regulate insulin secretion, glucokinase gene transcription and beta cell proliferation
- PFK-2/FBPase-2 protein rather than its product fructose 2,6-P(2) is the over-riding determinant of glucose-induced insulin secretion through regulation of glucokinase activity or subcellular targeting.
- Our study suggests that c.1253+8 C-->T polymorphism in intron 9 of glucokinase gene could have a role in predisposition to type 2 diabetes in women with gestational diabetes.
- Insulin, directly or indirectly, plays a role in placental growth, especially as a mutation in the GCK gene, which is known to only alter fetal insulin secretion.
- The polymorphism at -258 of the fetal hepatic glucokinase promoter is most probably not of a major relevance in the pathophysiology of low birth weight in preterm neonates.
- no difference in the frequencies of GCK polymorphisms between Czech diabetic (diabetes type 2, gestational diabetes) and non-diabetic populations
- Viallelic GCK loss should be considered as a potential cause permanent neonatal diabetes in children born to consanguineous parents.
- In a study of six missense mutations, mutation severity correlated with the importance of the glucokinase structural changes introduced by the mutations.
- Overexpression of glucokinase is unlikely to be a common cause of hypoglycaemia of infancy in humans.
- analysis of glucokinase by kinetic measurement and tryptophan fluorescence
- analysis of structural and genotype-phenotype analyses for glucokinase in MODY children from South Italy
- Results identify residue contacts in human glucokinase involved in the initial binding of alpha-d-glucose and conformational transitions.
- study found 2 novel (S76Y & N231S) & 13 previously reported (V62A, G72R, L146R, R191W, A208T, M210K, Y215X, M235T, R275C, E339G, R377C, S453L & IVS5+1G>C) GCK mutations in 23 maturity-onset diabetes of the young, type 2 probands & their 33 family members
- Glucose tolerance can remain stable over many years in subjects with type 2 diabetes due to relative stability of the glucokinase mutations.
- In the largest study performed to date on GCK in children with congenital hyperinsulinism, GCK mutations were found only in medically responsive children who were negative for ABCC8 and KCNJ11 mutations.
- In a population from southern Spain, carriers of the A allele of the -30G>A polymorphism in the promoter of the glucokinase gene had a lower risk for obesity and the likelihood of losing weight was greater in obese persons who had the A allele (GA or AA)
- analysis of a neonatal diabetes mellitus patient with a novel homozygous (T168A) glucokinase (GCK) mutation [case report]
- [Review] Increase in blood-glucose concentration in the portal vein activates glucokinase, first enzyme in the molecular pathway, causing an increase in concentration of glucose 6-phosphate, which modulates the phosphorylation state of downstream enzymes
- results suggested that mutations in MODY2 and MODY3 genes do not explain the majority of maturity-onset diabetes of the young (MODY) cases in Brazilian population
- HNF-4 and Foxo1 are required for reciprocal transcriptional regulation of glucokinase and glucose-6-phosphatase genes in response to fasting and feeding
- Prototypical activator of Glucokinase (GK) of the amino-heteroaryl-amide type bound to GK in a glucose-dependent manner and impaired the association of GK with GK regulatory protein
- This protein and glucokinase regulatory protein increase fasting blood glucose and risk of diabetics who have other risk factors.
- Eleven new activating mutations in the glucokinase gene have been discovered that are associated with persistent hyperinsulinemic hypoglycemia of infancy (PHHI). The stimulatory mutations described represent surreptitious genetic determinants of PHHI.