Hyperactive neuroendocrine secretion causes size, feeding, and metabolic defects of C. elegans Bardet-Biedl syndrome mutants.
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Conserved Genetic Interactions between Ciliopathy Complexes Cooperatively Support Ciliogenesis and Ciliary SignalingLoss of a neural AMP-activated kinase mimics the effects of elevated serotonin on fat, movement, and hormonal secretionsPrimary 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 ReservesBBS7 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.
P2860
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P2860
Hyperactive neuroendocrine secretion causes size, feeding, and metabolic defects of C. elegans Bardet-Biedl syndrome mutants.
description
2011 nî lūn-bûn
@nan
2011 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.
@ast
Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.
@en
Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.
@nl
type
label
Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.
@ast
Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.
@en
Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.
@nl
prefLabel
Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.
@ast
Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.
@en
Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.
@nl
P2093
P2860
P1433
P1476
Hyperactive neuroendocrine sec ...... Bardet-Biedl syndrome mutants.
@en
P2093
Daisy Wong
Kaveh Ashrafi
Supriya Srinivasan
P2860
P304
P356
10.1371/JOURNAL.PBIO.1001219
P407
P50
P577
2011-12-13T00:00:00Z