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Growth signaling and longevity in mouse models

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 rece...

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Detalles Bibliográficos
Autores principales: Kim, Seung-Soo, Lee, Cheol-Koo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Society for Biochemistry and Molecular Biology 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386229/
https://www.ncbi.nlm.nih.gov/pubmed/30545442
http://dx.doi.org/10.5483/BMBRep.2019.52.1.299
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author Kim, Seung-Soo
Lee, Cheol-Koo
author_facet Kim, Seung-Soo
Lee, Cheol-Koo
author_sort Kim, Seung-Soo
collection PubMed
description 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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spelling pubmed-63862292019-03-04 Growth signaling and longevity in mouse models Kim, Seung-Soo Lee, Cheol-Koo BMB Rep Invited Mini Review 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. Korean Society for Biochemistry and Molecular Biology 2019-01 2019-01-31 /pmc/articles/PMC6386229/ /pubmed/30545442 http://dx.doi.org/10.5483/BMBRep.2019.52.1.299 Text en Copyright © 2019 by the The Korean Society for Biochemistry and Molecular Biology This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Invited Mini Review
Kim, Seung-Soo
Lee, Cheol-Koo
Growth signaling and longevity in mouse models
title Growth signaling and longevity in mouse models
title_full Growth signaling and longevity in mouse models
title_fullStr Growth signaling and longevity in mouse models
title_full_unstemmed Growth signaling and longevity in mouse models
title_short Growth signaling and longevity in mouse models
title_sort growth signaling and longevity in mouse models
topic Invited Mini Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386229/
https://www.ncbi.nlm.nih.gov/pubmed/30545442
http://dx.doi.org/10.5483/BMBRep.2019.52.1.299
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