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Validated All-in-One™ qPCR Primer for GIP(NM_004123.2) Search again
Product ID:
HQP007406
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
-
Gene Description:
gastric inhibitory polypeptide
Target Gene Accession:
NM_004123.2(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
This gene encodes an incretin hormone and belongs to the glucagon superfamily. The encoded protein is important in maintaining glucose homeostasis as it is a potent stimulator of insulin secretion from pancreatic beta-cells following food ingestion and nutrient absorption. This gene stimulates insulin secretion via its G protein-coupled receptor activation of adenylyl cyclase and other signal transduction pathways. It is a relatively poor inhibitor of gastric acid secretion. [provided by RefSeq].
Gene References into function
- Substitution of Glu(3) in GIP with proline produces a novel dipeptidylpeptidase IV-resistant GIP antagonist which inhibits GIP-induced cAMP generation and insulin secretion with high sensitivity and specificity in vitro.
- activates the Raf-Mek1/2-ERK1/2 module via a cyclic AMP/cAMP-dependent protein kinase/Rap1-mediated pathway
- Mutation in promoter region of gip receptor gene are unlikely to underlie GIP-dependent Cushing syndrome.
- delayed elimination in renal insufficiency
- Elevated plasma GIP levels are correlated with hyperinsulinemia in the impaired glucose-tolerant state, whereas type 2 diabetes is associated with a failure to secrete adequate amounts of GIP.
- bombesin and nutrients additively stimulate GIP release from GIP/Ins cells.
- Results describe the solution structure of GIP(1-30)amide, the major biologically active fragment of glucose-dependent insulinotropic polypeptide.
- GIP augments glucose-stimulated insulin secretion and acts as an endogenous inhibitor of gastric acid secretion--REVIEW
- Reduced secretion or action of GLP-1 or GIP does not explain a relative reduced beta-cell responsiveness to glucose or the slightly elevated plasma glucose concentrations observed in young low birth weight men
- GIP stimulates insulin secretion by potentiating events underlying membrane depolarization and exerting direct effects on exocytosis.
- The relationship between insulin resistance and the insulin secretion to GIP suggests that beta cell secretory function in response to different stimuli increases adaptively when insulin sensitivity is diminished, as in gestational diabetes.
- GIP is rapidly degraded into inactive metabolites by the enzyme dipeptidyl-peptidase-IV. (review)
- protein kinase B, LKB1, and AMP-activated protein kinase have roles in activation of lipoprotein lipase by glucose-dependent insulinotropic polypeptide in adipocytes
- An inverse relationship between insulin concentrations and insulin clearance suggests that the secretion of insulin itself determines the rate of hepatic insulin clearance.
- study identified a splice site mutation of the Glucose-dependent insulinotropic polypeptide (GIP) gene which results in a truncated protein and provides evidence for association of GIP receptor genotype with cardiovascular disease
- physiologic role for GIP in lipid homeostasis and possibly in the pathogenesis of obesity.
- concomitant expression of Pax6 and Pdx1 is important for glucose-dependent insulinotropic polypeptide expression