Hyperactive neuroendocrine secretion causes size, feeding, and metabolic defects of C. elegans Bardet-Biedl syndrome mutants. - Wikidata - wikimedia - TriplyDB

Hyperactive neuroendocrine secretion causes size, feeding, and metabolic defects of C. elegans Bardet-Biedl syndrome mutants.

Hyperactive neuroendocrine secretion causes size, feeding, and metabolic defects of C. elegans Bardet-Biedl syndrome mutants.

http://www.wikidata.org/entity/Q34105144

about

Conserved Genetic Interactions between Ciliopathy Complexes Cooperatively Support Ciliogenesis and Ciliary Signaling Loss of a neural AMP-activated kinase mimics the effects of elevated serotonin on fat, movement, and hormonal secretions Primary cilia in pancreatic development and disease.Identification and characterization of a novel allele of Caenorhabditis elegans bbs-7.QTL analysis of dietary obesity in C57BL/6byj X 129P3/J F2 mice: diet- and sex-dependent effects.Kynurenic acid is a nutritional cue that enables behavioral plasticity.Whole organism transcriptome analysis of zebrafish models of Bardet-Biedl Syndrome and Alström Syndrome provides mechanistic insight into shared and divergent phenotypes.Differential effects on β-cell mass by disruption of Bardet-Biedl syndrome or Alstrom syndrome genes.Cell-cycle quiescence maintains Caenorhabditis elegans germline stem cells independent of GLP-1/Notch.C. elegans Body Cavity Neurons Are Homeostatic Sensors that Integrate Fluctuations in Oxygen Availability and Internal Nutrient Reserves BBS7 is required for BBSome formation and its absence in mice results in Bardet-Biedl syndrome phenotypes and selective abnormalities in membrane protein trafficking.Insights and challenges in using C. elegans for investigation of fat metabolism.Metabolic regulation and energy homeostasis through the primary Cilium.From phenologs to silent suppressors: Identifying potential therapeutic targets for human disease.Investigating Connections between Metabolism, Longevity, and Behavior in Caenorhabditis elegans.Genetic kidney diseases: Caenorhabditis elegans as model system.A new tool in C. elegans reveals changes in secretory protein metabolism in ire-1-deficient animals.Ciliary dysfunction impairs beta-cell insulin secretion and promotes development of type 2 diabetes in rodents.UNC-18 and Tomosyn Antagonistically Control Synaptic Vesicle Priming Downstream of UNC-13 in Caenorhabditis elegans.Kynurenic acid accumulation underlies learning and memory impairment associated with aging.

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Hyperactive neuroendocrine secretion causes size, feeding, and metabolic defects of C. elegans Bardet-Biedl syndrome mutants.

http://www.wikidata.org/entity/Q34105144

description

2011 nî lūn-bûn

@nan

2011 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

@zh-hk

2011年論文

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2011年論文

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2011年论文

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name

Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.

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Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.

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Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.

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type

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Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.

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Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.

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Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.

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prefLabel

Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.

@ast

Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.

@en

Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.

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P356

JOURNAL.PBIO.1001219

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Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.

@en

P2093

Daisy Wong

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

Jason Liu

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Kaveh Ashrafi

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Supriya Srinivasan

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P2860

Basal body dysfunction is a likely cause of pleiotropic Bardet-Biedl syndrome

Bardet-Biedl syndrome genes are important in retrograde intracellular trafficking and Kupffer's vesicle cilia function

A core complex of BBS proteins cooperates with the GTPase Rab8 to promote ciliary membrane biogenesis

Requirement of Bardet-Biedl syndrome proteins for leptin receptor signaling

The conserved Bardet-Biedl syndrome proteins assemble a coat that traffics membrane proteins to cilia

The genetics of Caenorhabditis elegans

Loss of C. elegans BBS-7 and BBS-8 protein function results in cilia defects and compromised intraflagellar transport

Regulation of DAF-2 receptor signaling by human insulin and ins-1, a member of the unusually large and diverse C. elegans insulin gene family

Serotonin regulates C. elegans fat and feeding through independent molecular mechanisms

Loss of Bardet Biedl syndrome proteins causes defects in peripheral sensory innervation and function

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e1001219

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scholarly article

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10.1371/JOURNAL.PBIO.1001219

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12

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51899259

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22180729

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Caenorhabditis elegans

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3236739

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