2 edition of Characterisation of insulin gene regulatory proteins found in the catalog.
Characterisation of insulin gene regulatory proteins
Martin Lucas Read
Thesis (Ph.D.) - University of Birmingham, Department of Medicine, Faculty of Medicine and Dentistry.
|Statement||by Martin Lucas Read.|
The production of biopharmaceutical proteins by the mammary glands of genetically modified transgenic cows (dairy pharming) is currently under extensive exploration because it promises to provide high quality therapeutic medicine for humans at an acceptable cost. However, production of transgenic cows is still a costly process and the success rate is low. This is the Third Servier-IGIS Symposium Diabetes Supplement. As members of the International Group on Insulin Secretion (IGIS), we have done the utmost to fulfill the promise made at the First Servier-IGIS Symposium (1): the provision of yearly symposia of the highest scientific significance dealing with insulin secretion, β-cell biology, and islet by: 3.
Glucose-stimulated insulin gene transcription is mainly regulated by a bp promoter region upstream of the transcription start site by beta-cell-enriched transcription factors Pdx-1, MafA, and NeuroD1. Previous studies have shown that histone H4 hyperacetylation is important for acute up-regulation of insulin gene by: 7. • An operon includes 1. The adjacent structural genes that code for the related enzymes or associated proteins. 2. A regulatory gene that encodes a repressor protein which binds to the operator site. 3. Control elements that are the sites on the DNA near the structural genes, at which regulatory proteins act.
Glucose effects on gene expression have traditionally been ascribed to its regulation of insulin release from the pancreatic β-cell. However, studies with primary hepatocytes and pancreatic β-cells have shown that glucose acts independently of insulin to control gene expression. Characterization of somatostatin transactivating factor-1, a novel homeobox factor that stimulates somatostatin expression in pancreatic islet cells. Mol Endocrinol of HIT cells to high glucose concentrations paradoxically decreases insulin gene transcription and alters binding of insulin gene regulatory protein.
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The phosphatase inhibitor, okadaic acid, mimics the action of insulin on PEPCK gene transcription suggesting that, as with most of insulin's actions, changes in protein phosphorylation are involved in these effects.
Indeed, regulation of PEPCK gene transcription by insulin Cited by: 2. Regular Article. Regulation of insulin gene transcription. Abstract. Recent studies of the insulin gene promoter and the transcription factors that regulate it have expanded our understanding of both how the production of insulin is restricted to the pancreatic β -cell, and how that production is regulated by physiologic signals such as by: Boam DS, Clark AR, Docherty K.
Positive and negative regulation of the human insulin gene by multiple trans-acting factors. J Biol Chem. May 15; (14)–  [Google ScholarKarlsson O, Walker MD, Rutter WJ, Edlund T.
Individual protein-binding domains of the insulin gene enhancer positively activate beta-cell-specific by: Regulation of insulin gene transcription. Abstract. Selective transcription of the insulin gene in pancreatic β cells is regulated by its enhancer, located between nucleotides to relative to the transcription start site.
The activity o f the enhancer is controlled by both positive- Cited by: Part of the Handbook of Experimental Pharmacology book series (HEP, volume 92) Insulin genes from several mammalian species have been isolated and characterized.
This has permitted significant progress towards understanding the mechanisms involved in regulation of expression of the by: 1. Humans have a single insulin gene, INS (rodents have two, ins1 and ins2), located on chromos the transcription of which is controlled largely by upstream enhancer elements that bind key.
The insulin gene is expressed exclusively in the beta cells of the islet of Langerhans. The release of this polypeptide hormone into Characterisation of insulin gene regulatory proteins book blood- stream, principally in response to elevated glucose levels, is essential for controlling carbohydrate metabolism in peripheral tissues.
INSULIN GENE TRANSCRIPTION in the β-cells of the pancreas is up-regulated by increases in blood glucose levels. β-Cell-specific expression and glucose stimulation of the human insulin gene in the pancreas are mediated by upstream sequences within the region −90 to − relative to the transcription start site (1–4).Several transcription factors such as Pdx-1 and MafA (Ripe3b1) Cited by: Karlsson O, Thor S, Norberg T, Ohlsson H, Edlund T: Insulin gene enhancer binding protein isl-1 is a member of a novel class of proteins containing both a homeo-and a cys-his domain.
Nature –, Cited by: 4. Insulin and its related proteins have been shown to be produced inside the brain, and reduced levels of these proteins are linked to Alzheimer's disease. Insulin release is stimulated also by beta-2 receptor stimulation and inhibited by alpha-1 receptor s: INS, IDDM, IDDM1, IDDM2, ILPR.
tentially inhibitory, regulatory factors in the glucotoxic impair-ment of insulin gene transcription in pancreatic b cells. We have identified the basic leucine zipper transcription factor CCAAT/enhancer–binding protein b (C/EBP b) as such a neg-ative regulatory factor on insulin gene transcription in pancre-atic b cells (10).
To determine the mechanism underlying regulation of the insulin gene by Pdx-1, we performed a kinetic analysis of insulin transcription following adenovirus-mediated delivery of a small interfering RNA specific for pdx-1 into insulinoma cells and pancreatic islets to diminish endogenous Pdx-1 protein.
Insulin (from Latin insula, island) is a peptide hormone produced by beta cells of the pancreatic islets; it is considered to be the main anabolic hormone of the body.
It regulates the metabolism of carbohydrates, fats and protein by promoting the absorption of carbohydrates, especially glucose from the blood into liver, fat and skeletal muscle cells.
In these tissues the absorbed glucose is Aliases: INS, IDDM, IDDM1, IDDM2, ILPR. Insulin is a protein released by the human pancreas to cope with rising blood sugar levels.
The release of insulin from pancreatic cells causes fat cells elsewhere in the body to take up glucose from the blood. A man with normal blood sugar regulation abilities eats several sugary donuts.
Glucose regulation of insulin gene expression. Glucose is the major nutrient regulator of pancreatic β-cell function and coordinately regulates insulin gene expression, insulin biosynthesis, and insulin secretion. Glucose controls all steps of insulin gene expression, including transcription, preRNA splicing, and mRNA by: Fig.
1 Promoter of the rat insulin 1 gene, indicating key cis-acting elements together with BETA2, E2A and PDX1 (IPF1) the major transcription factors implicated in cell-specific transcription of the insulin gene. Also shown is HNF4α with its proposed binding site (shown in blue) and consensus binding sequence.
michael_walker 12/26/01, PM. THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. No. 35, Issue of Decem pp. Printed in U. S.A. Regulation of Insulin Receptor Gene Expression CELL CYCLE-MEDIATED EFFECTS ON INSULIN RECEPTOR mRNA STABILITY* (Received for publication, July 7, ) James R.
Levy$ and Victoria Hug. Mechanism of action: The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver.
It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Defective regulation of gene expression may be involved in the pathogenesis of type 2 diabetes.
We have characterized the concerted regulation by insulin (3-h hyperinsulinemic clamp) of the expression of 10 genes related to insulin action in skeletal muscle and in subcutaneous adipose tissue, and we have verified whether a defective regulation of some of them could be specifically Cited by: Start studying BIO chp 10 Qs.
Learn vocabulary, terms, and more with flashcards, games, and other study tools. A mutation in the gene for insulin results in a protein with a drastically distorted three-dimensional shape. What is the most likely outcome.
-the gene could have abnormal regulation -the gene could be permanently turned on. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 thereby activating mTORC1 pathway.
The Ras/RAF/MAP2K/MAPK pathway is mainly involved in mediating cell growth, survival and cellular differentiation of insulin. Phosphorylated IRS1 recruits GRB2/SOS complex, which triggers the activation of the Ras/RAF/MAP2K/MAPK pathway. We have recently shown that the human insulin gene promoter makes physical contact in pancreatic islet cells with many distant sites on the same chromosome.
Some of these contacts are to genes that are important in insulin secretion, and their expression is stimulated by the contacts, which increase when glucose is added to the islets.IRS4 (Insulin Receptor Substrate 4) is a Protein Coding gene. Diseases associated with IRS4 include Hypothyroidism, Congenital, Nongoitrous, 9 and its related pathways are Autophagy - animal and Signaling by Ontology (GO) annotations related to this gene include obsolete signal transducer activity and insulin receptor binding.