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Validated All-in-One™ qPCR Primer for GCG(NM_002054.4) Search again
Product ID:
HQP007233
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
GLP-1, GLP1, GLP2, GRPP
Gene Description:
glucagon
Target Gene Accession:
NM_002054.4(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
The protein encoded by this gene is actually a preproprotein that is cleaved into four distinct mature peptides.
Gene References into function
- low secretion of GLP-1 in girls with obesity may seriously and negatively influence the course of this disease while low levels in girls with anorexia nervosa are beneficial and promote appetite
- present in human colorectal adenocarcinomas and liver metastases
- role of polarity at Asp198 in determining binding site for glucagon-like peptide-1 receptor
- There are interactions between this protein, specific NEFA and insulin secretion
- some of the events that lead to the differentiation of pancreatic ductal cells in response to treatment with human GLP-1
- conclude that the elimination of GLP-1 is the same in obese type 2 diabetic petients and matched healthy subjects
- The isolated N-terminal domain of the glucagon-like peptide-1 (GLP-1) receptor binds exendin peptides with much higher affinity than GLP-1.
- leptin stimulates GLP-1 secretion from rodent and human intestinal L cells; leptin resistance may account for the decreased levels of GLP-1 found in obese humans
- single treatment of sensitized mice with GLP diminishes both immediate and late-phase hypersensitivity reactions characteristic of food allergy by inhibiting transepithelial uptake of antigen
- role of M1 and M2 muscarinic receptors expressed by human L cells in the control of GLP-1 secretion.
- GLP-1 improves function and inhibit apoptosis in freshly isolated human islets.
- GLP-1 has to be present in blood to stimulate insluin or suppress glucagon. Human pancreatic beta cells do not appear to possess memory for insulinotropic stimuli.
- GLP-2 may prove to be important in the attempt to optimize remnant intestinal function thereby eliminating the need for parenteral support in short bowel syndrome.
- Review article focuses on the complex integrative mechanisms that regulate the secretion of GLP-1 and GLP-2 from intestinal L cells, including both direct and indirect regulation by ingested nutrients.
- delayed elimination in renal insufficiency
- In morbid obesity, accelerated inactivation of circulating GLP-1 could at least partially account for plasma peptide levels lower than normal, defective availability of such a satiety factor possibly contributing to eating behaviour abnormalities.
- Increased GLP-1 levels, which lead to decreased food intake, may also contribute to the weight loss that is associated with the use of this drug in obese diabetics.
- GLP-1 and GLP-2 exhibit a diverse array of metabolic, proliferative and cytoprotective actions with important clinical implications for the treatment of diabetes and gastrointestinal disease--REVIEW
- GLP-1 protects against myocardial infarction in the isolated and intact rat heart.
- GLP-1, like insulin, stimulates glucose uptake in myocytes, and this involves activation of PI3K/PKB, p44/42 MAPKs, partially p70s6k, and possibly PKC
- Review. Summarizes signaling properties of GLP-1 that may explain its ability to increase beta-cell mass, to increase pancreatic insulin secretory capacity, and to lower levels of blood glucose in type 2 diabetic subjects.
- Results demonstrate that glucagon like peptide-1 is capable of preserving beta-cell function and protecting cells from apoptotic cell death.
- in overweight/obese subjects, glucagon-like peptide 1 concentrations after weight loss were decreased compared with before weight loss, and nutrient-related stimulation was abolished
- 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
- The glucose-lowering effect of GLP-1 is markedly reduced when the deceleration of gastric emptying is antagonized, illustrating the importance of this facet of the multiple antidiabetic actions of GLP-1.
- important role for the irregularities in glucagon response in the postprandial glucose excursion in glucose intolerance and type 2 diabetes
- Glucagon inhibits ghrelin secretion in humans.
- GLP-1 has the potential to improve both alpha cell and beta cell function, and could be of benefit in patients with a broad range of metabolic disorders. (review)
- GLP-1 is preserved in type 2 diabetic patients, this peptide was a candidate as a therapeutic agent for this disease. (review)
- GLP-1 may be another important determiner of pancreatic endocrine differentiation as is pdx-1
- glicentin plays an important role in the regulating inhibition of the contraction reaction in normal human jejunum via NANC nerves, and has a direct action on the jejunal muscle receptor.
- GLP-1 suppresses glucagon secretion, promotes satiety, delays gastric emptying and stimulates peripheral glucose uptake. Because of its multiple actions, GLP-1 is an attractive therapeutic target for the treatment of type 2 diabetes[review]
- The body adapts to insulin resistance by increasing the glucagon response to arginine and by increasing the suppression of glucagon levels by glucose.
- GLP-2 reduces gastric acid secretion but does not seem to have an influence on gastric emptying
- the effects of intraduodenal fatty acids on ghrelin, PYY and GLP-2 secretion are dependent on their chain length
- Glucagon suppression of ghrelin secretion is exerted at the hypothalamus-pituitary level.
- Review summarizes the appetite suppressing effects of GLP-1 in the regulation of food intake, focusing on whether it is a true endocrine factor that acts as a physiologic, hormonal regulator of appetite.
- Activin A has opposite effects on glucagon and arx gene expression in alpha-cells compared with beta-cells, a finding that may have relevance during pancreatic endocrine lineage specification and physiological function of the adult islets
- These data suggest mechanistic similarities in the nucleation behaviour of different amyloid-like fibrils and aggregates.
- Amino acid-enhanced secretion of glucagon in response to hypoglycaemia remains under physiological control since it is regulated primarily by the ambient plasma glucose concentration.
- regeneration of insulin-producing cells by GLP-1 gene therapy may be a potential method for prolonged control of type 1 diabetes in humans
- These data are consistent with the hypothesis that nitric oxide partly mediates the effects of GLP-1 on postprandial but not fasting gastric volumes in humans.
- Novel regulatory element in the human proglucagon proximal promoter, located between the G2 and G3 enhancer elements.
- GLP-2 is present in human cord blood by the time of birth. The level of GLP-2 is comparable to adult fasting levels. Spontaneous birth at most induces a minor increase in GLP-2 in term infants.
- An inverse relationship between insulin concentrations and insulin clearance suggests that the secretion of insulin itself determines the rate of hepatic insulin clearance.
- Transgenic GLP-1 stimulates the electrical activity of hypothalamic proopiomelanocortin neurons by activation of protein kinase A and a subsequent increase in L-type calcium current.
- secretion of glucagon-like peptide-1 is regualted by gustducin and sweet taste receptors.
- Insulin resistance is independently associated with raised fasting plasma glucagon and proinsulin concentrations.
- Pax-6 and c-Maf interact with G1 to activate basal expression of the glucagon gene
- Since hepatic glycogen synthesis, a GLP-1 action, was impaired, the altered expressions of GLP-1 and DPPIV may be involved in the development of HCV-associated glucose intolerance.
- Reduced GLP1 levels are seen in all groups with abnormal glucose tolerance and are unrelated to the insulin release pattern during an intravenous glucose tolerance test.
- observations suggest that Glucagon-like peptide-1 (GLP-1) inhibits tumour necrosis factor-alpha (TNF-alpha)-mediated plasmogen activator inhibitor-1 (PAI-1)induction in vascular endothelial cells
- tested the hypothesis that gender and BMI interact to produce differences in postprandial secretion of selected humoral markers implicated in hunger and satiety(blood glucose, insulin, leptin, ghrelin, glucagon-like peptide-1, and glucagon)
- Lower concentrations of GLP-1, a satiety hormone, in overweight compared to normal weight male adolescents support the theory that GLP-1 plays a role in the etiology of overweight.
- Gut peptide GLP-1 decreases motility in the antro-duodeno-jejunal region and inhibits migrating motor complexes in healthy subjects and patients with irritable bowel syndrome.
- Mutated GLP-1 exhibited neuronal protection properties.
- Enteral nutrients potentiate the intestinotrophic action of glucagon-like peptide-2 in association with increased insulin-like growth factor-I responses in rats.