Central nervous system imprinting of the G protein G(s)alpha and its role in metabolic regulation. - Wikidata - awgldk - TriplyDB

Central nervous system imprinting of the G protein G(s)alpha and its role in metabolic regulation.

Central nervous system imprinting of the G protein G(s)alpha and its role in metabolic regulation.

http://www.wikidata.org/entity/Q37233680

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The GNAS complex locus and human diseases associated with loss-of-function mutations or epimutations within this imprinted gene Gene Dosage Effects at the Imprinted Gnas Cluster Biphasic effect of melanocortin agonists on metabolic rate and body temperature Maternal inheritance of the Gnas cluster mutation Ex1A-T affects size, implicating NESP55 in growth Gsα deficiency in the dorsomedial hypothalamus underlies obesity associated with Gsα mutations.Gsα Deficiency in the Ventromedial Hypothalamus Enhances Leptin Sensitivity and Improves Glucose Homeostasis in Mice on a High-Fat Diet.An essential role for the K+-dependent Na+/Ca2+-exchanger, NCKX4, in melanocortin-4-receptor-dependent satiety.Leptin and the systems neuroscience of meal size control.G(s)alpha deficiency in adipose tissue leads to a lean phenotype with divergent effects on cold tolerance and diet-induced thermogenesis Rare Variant Analysis of Human and Rodent Obesity Genes in Individuals with Severe Childhood Obesity.Mammalian genomic imprinting.The role of GNAS and other imprinted genes in the development of obesity.Bone mineral density in pseudohypoparathyroidism type 1a.Postnatal changes in the expression pattern of the imprinted signalling protein XLαs underlie the changing phenotype of deficient mice.Loss of Gnas imprinting differentially affects REM/NREM sleep and cognition in mice.Eating behaviors in obese children with pseudohypoparathyroidism type 1a: a cross-sectional study.The role of genomic imprinting in biology and disease: an expanding view.A mouse model for osseous heteroplasia Lack of cAMP-response element-binding protein 1 in the hypothalamus causes obesity.Evidence of hormone resistance in a pseudo-pseudohypoparathyroidism patient with a novel paternal mutation in GNAS.Effects of deficiency of the G protein Gsα on energy and glucose homeostasis Genetic approaches to understanding human obesity.GNAS Spectrum of Disorders.Ablation of the transcriptional regulator Id1 enhances energy expenditure, increases insulin sensitivity, and protects against age and diet induced insulin resistance, and hepatosteatosis.New mutations at the imprinted Gnas cluster show gene dosage effects of Gsα in postnatal growth and implicate XLαs in bone and fat metabolism but not in suckling.Gsα deficiency in the paraventricular nucleus of the hypothalamus partially contributes to obesity associated with Gsα mutations G(q/11)α and G(s)α mediate distinct physiological responses to central melanocortins Non-Coding RNAs at the Gnas and Snrpn-Ube3a Imprinted Gene Loci and Their Involvement in Hereditary Disorders.Resting Energy Expenditure Is Decreased in Pseudohypoparathyroidism Type 1A.Energy expenditure in obese children with pseudohypoparathyroidism type 1a Reductions in hypothalamic Gfap expression, glial cells and α-tanycytes in lean and hypermetabolic Gnasxl-deficient mice Paternal GNAS mutations lead to severe intrauterine growth retardation (IUGR) and provide evidence for a role of XLαs in fetal development.Reduced insulin sensitivity in adults with pseudohypoparathyroidism type 1a.Neural melanocortin receptors in obesity and related metabolic disorders.New Perspectives on Genomic Imprinting, an Essential and Multifaceted Mode of Epigenetic Control in the Developing and Adult Brain.Melanocortin-4 receptor-regulated energy homeostasis A survey of tissue-specific genomic imprinting in mammals.Pro-Opiomelanocortin (POMC) Neurones, POMC-Derived Peptides, Melanocortin Receptors and Obesity: How Understanding of this System has Changed Over the Last Decade.Methylation and transcripts expression at the imprinted GNAS locus in human embryonic and induced pluripotent stem cells and their derivatives.The Role of the Melanocortin System in Metabolic Disease: New Developments and Advances.

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Central nervous system imprinting of the G protein G(s)alpha and its role in metabolic regulation.

http://www.wikidata.org/entity/Q37233680

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

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scientific article published on June 2009

@en

vedecký článok

@sk

vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

@cs

name

Central nervous system imprinting of the G protein G

@nl

Central nervous system imprint ...... role in metabolic regulation.

@en

type

label

Central nervous system imprinting of the G protein G

@nl

Central nervous system imprint ...... role in metabolic regulation.

@en

prefLabel

Central nervous system imprinting of the G protein G

@nl

Central nervous system imprint ...... role in metabolic regulation.

@en

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J.CMET.2009.05.004

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Cell Metabolism

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Central nervous system imprint ...... role in metabolic regulation.

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Divakar Gupta

http://www.w3.org/2001/XMLSchema#string

Edwin W Lai

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James Kelleher

http://www.w3.org/2001/XMLSchema#string

Jie Wang

http://www.w3.org/2001/XMLSchema#string

Kathryn E Dickerson

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Lee S Weinstein

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Min Chen

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Oksana Gavrilova

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Tao Xie

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P2860

Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene

Cognitive impairment is prevalent in pseudohypoparathyroidism type Ia, but not in pseudopseudohypoparathyroidism: possible cerebral imprinting of Gsalpha

Body mass index differences in pseudohypoparathyroidism type 1a versus pseudopseudohypoparathyroidism may implicate paternal imprinting of Galpha(s) in the development of human obesity

Targeted disruption of the melanocortin-4 receptor results in obesity in mice

Central melanocortin receptors regulate insulin action

Paternal versus maternal transmission of a stimulatory G-protein alpha subunit knockout produces opposite effects on energy metabolism

Disruption of the glucocorticoid receptor gene in the nervous system results in reduced anxiety

Alternative Gnas gene products have opposite effects on glucose and lipid metabolism.

Genomic imprinting and kinship: how good is the evidence?

SIM1 overexpression partially rescues agouti yellow and diet-induced obesity by normalizing food intake.

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548-555

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scholarly article

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10.1016/J.CMET.2009.05.004

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6

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9

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2009-06-01T00:00:00Z

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26261486

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19490909

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2698878

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