A model for obesity and gigantism due to disruption of the Ankrd26 gene
DC Field | Value | Language |
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dc.contributor.author | Bera, Tapan K. | - |
dc.contributor.author | Liu, Xiu-Fen | - |
dc.contributor.author | Yamada, Masanori | - |
dc.contributor.author | Gavrilova, Oksana | - |
dc.contributor.author | Mezey, Eva | - |
dc.contributor.author | Tessarollo, Lino | - |
dc.contributor.author | Anver,Miriam | - |
dc.contributor.author | Hahn, Yoonsoo | - |
dc.contributor.author | Lee,Byungkook | - |
dc.contributor.author | Pastan, Ira | - |
dc.date.available | 2019-05-30T05:37:21Z | - |
dc.date.issued | 2008-01 | - |
dc.identifier.issn | 0027-8424 | - |
dc.identifier.issn | 1091-6490 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/23879 | - |
dc.description.abstract | Obesity is a major health hazard that is caused by a combination of genetic and behavioral factors. Several models of obesity have been described in mice that have defects in the production of peptide hormones, in the function of cell membrane receptors, or in a transcription factor required for neuronal cell development. Wehave been investigating the function of a family of genes (POTE and ANKRD26) that encode proteins that are associated with the inner aspect of the cell membrane and that contain both ankyrin repeats and spectrin helices, motifs known to interact with signaling proteins in the cell. To assess the function of ANKRD26, we prepared a mutant mouse with partial inactivation of the Ankrd26 gene. We find that the homozygous mutant mice develop extreme obesity, insulin resistance, and an increase in body size. The obesity is associated with hyperphagia with no reduction in energy expenditure and activity. The Ankrd26 protein is expressed in the arcuate and ventromedial nuclei within the hypothalamus and in the ependyma and the circumventricular organs that act as an interface between the peripheral circulation and the brain. In the enlarged hearts of the mutant mice, the levels of both phospho-Akt and mTOR were elevated. These results show that alterations in an unidentified gene can lead to obesity and identify a molecular target for the treatment of obesity. | - |
dc.format.extent | 6 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | NATL ACAD SCIENCES | - |
dc.title | A model for obesity and gigantism due to disruption of the Ankrd26 gene | - |
dc.type | Article | - |
dc.identifier.doi | 10.1073/pnas.0710978105 | - |
dc.identifier.bibliographicCitation | Proceedings of the National Academy of Sciences of the United States of America, v.105, no.1, pp 270 - 275 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.wosid | 000252435300051 | - |
dc.identifier.scopusid | 2-s2.0-38349111383 | - |
dc.citation.endPage | 275 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 270 | - |
dc.citation.title | Proceedings of the National Academy of Sciences of the United States of America | - |
dc.citation.volume | 105 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordAuthor | Akt signaling | - |
dc.subject.keywordAuthor | Coiled-coil motif | - |
dc.subject.keywordAuthor | Hyperphagia | - |
dc.subject.keywordAuthor | Insulin resistance | - |
dc.subject.keywordAuthor | POTE ancestor | - |
dc.subject.keywordPlus | animal experiment | - |
dc.subject.keywordPlus | animal model | - |
dc.subject.keywordPlus | arcuate nucleus | - |
dc.subject.keywordPlus | article | - |
dc.subject.keywordPlus | body size | - |
dc.subject.keywordPlus | cell membrane | - |
dc.subject.keywordPlus | controlled study | - |
dc.subject.keywordPlus | energy expenditure | - |
dc.subject.keywordPlus | female | - |
dc.subject.keywordPlus | gene disruption | - |
dc.subject.keywordPlus | gene function | - |
dc.subject.keywordPlus | gigantism | - |
dc.subject.keywordPlus | hyperphagia | - |
dc.subject.keywordPlus | hypothalamus | - |
dc.subject.keywordPlus | insulin resistance | - |
dc.subject.keywordPlus | male | - |
dc.subject.keywordPlus | mouse | - |
dc.subject.keywordPlus | nonhuman | - |
dc.subject.keywordPlus | obesity | - |
dc.subject.keywordPlus | peripheral circulation | - |
dc.subject.keywordPlus | priority journal | - |
dc.subject.keywordPlus | protein expression | - |
dc.subject.keywordPlus | thalamus ventral nucleus | - |
dc.subject.keywordPlus | Animals | - |
dc.subject.keywordPlus | Body Size | - |
dc.subject.keywordPlus | Chromosome Mapping | - |
dc.subject.keywordPlus | Disease Models, Animal | - |
dc.subject.keywordPlus | DNA, Complementary | - |
dc.subject.keywordPlus | DNA-Binding Proteins | - |
dc.subject.keywordPlus | Exons | - |
dc.subject.keywordPlus | Expressed Sequence Tags | - |
dc.subject.keywordPlus | Genotype | - |
dc.subject.keywordPlus | Gigantism | - |
dc.subject.keywordPlus | Homozygote | - |
dc.subject.keywordPlus | Humans | - |
dc.subject.keywordPlus | Insulin Resistance | - |
dc.subject.keywordPlus | Mice | - |
dc.subject.keywordPlus | Mice, Inbred C57BL | - |
dc.subject.keywordPlus | Models, Genetic | - |
dc.subject.keywordPlus | Mutation | - |
dc.subject.keywordPlus | Obesity | - |
dc.subject.keywordPlus | Transcription Factors | - |
dc.subject.keywordPlus | Mus | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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