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Growth signaling and longevity in mouse models

Authors
Kim, Seung-SooLee, Cheol-Koo
Issue Date
31-1월-2019
Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
Keywords
Gene expression; Growth signaling; Longevity; Mouse model
Citation
BMB REPORTS, v.52, no.1, pp.70 - 85
Indexed
SCIE
SCOPUS
KCI
Journal Title
BMB REPORTS
Volume
52
Number
1
Start Page
70
End Page
85
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/68224
DOI
10.5483/BMBRep.2019.52.1.299
ISSN
1976-6696
Abstract
Reduction of insulin/insulin-like growth factor 1 (IGF1) signaling (IIS) extends the lifespan of various species. So far, several longevity mouse models have been developed containing mutations related to growth signaling deficiency by targeting growth hormone (GH), IGF1, IGF1 receptor, insulin receptor, and insulin receptor substrate. In addition, p70 ribosomal protein S6 kinase 1 (S6K1) knockout leads to lifespan extension. S6K1 encodes an important kinase in the regulation of cell growth. S6K1 is regulated by mechanistic target of rapamycin (mTOR) complex 1. The v-myc myelocytomatosis viral oncogene homolog (MYC)-deficient mice also exhibits a longevity phenotype. The gene expression profiles of these mice models have been measured to identify their longevity mechanisms. Here, we summarize our knowledge of long-lived mouse models related to growth and discuss phenotypic characteristics, including organ-specific gene expression patterns.
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