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rdf:type |
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lifeskim:mentions |
umls-concept:C0017725,
umls-concept:C0020663,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0027882,
umls-concept:C0027893,
umls-concept:C0299583,
umls-concept:C0392747,
umls-concept:C0443172,
umls-concept:C1150593,
umls-concept:C1546857
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pubmed:issue |
1
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pubmed:dateCreated |
2006-12-29
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pubmed:abstractText |
Changes in the activity of glucose-excited and glucose-inhibited neurons within the basomedial hypothalamus are key to the central regulation of satiety. However, the molecular mechanisms through which these cells respond to extracellular stimuli remain poorly understood. Here, we investigate the role of 5'-AMP-activated protein kinase (AMPK), a trimeric complex encoded by seven distinct genes of the PRKA family, in the responses to glucose and leptin of each cell type.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/(6-(4-(2-piperidin-1-ylethoxy)phenyl...,
http://linkedlifedata.com/resource/pubmed/chemical/AICA ribonucleotide,
http://linkedlifedata.com/resource/pubmed/chemical/AMP-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Aminoimidazole Carboxamide,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Hypoglycemic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/Multienzyme Complexes,
http://linkedlifedata.com/resource/pubmed/chemical/Neuropeptide Y,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrimidines,
http://linkedlifedata.com/resource/pubmed/chemical/Ribonucleotides
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0012-186X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
50
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
168-77
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17093945-AMP-Activated Protein Kinases,
pubmed-meshheading:17093945-Aminoimidazole Carboxamide,
pubmed-meshheading:17093945-Animals,
pubmed-meshheading:17093945-Calcium,
pubmed-meshheading:17093945-Cells, Cultured,
pubmed-meshheading:17093945-Dose-Response Relationship, Drug,
pubmed-meshheading:17093945-Glucose,
pubmed-meshheading:17093945-Hypoglycemic Agents,
pubmed-meshheading:17093945-Hypothalamus,
pubmed-meshheading:17093945-Leptin,
pubmed-meshheading:17093945-Membrane Potentials,
pubmed-meshheading:17093945-Multienzyme Complexes,
pubmed-meshheading:17093945-Neurons,
pubmed-meshheading:17093945-Neuropeptide Y,
pubmed-meshheading:17093945-Patch-Clamp Techniques,
pubmed-meshheading:17093945-Protein-Serine-Threonine Kinases,
pubmed-meshheading:17093945-Pyrazoles,
pubmed-meshheading:17093945-Pyrimidines,
pubmed-meshheading:17093945-Rats,
pubmed-meshheading:17093945-Rats, Wistar,
pubmed-meshheading:17093945-Ribonucleotides
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pubmed:year |
2007
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pubmed:articleTitle |
Inhibition by glucose or leptin of hypothalamic neurons expressing neuropeptide Y requires changes in AMP-activated protein kinase activity.
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pubmed:affiliation |
Henry Wellcome Laboratories of Integrated Cell Signalling and Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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