Role of CBP and SATB-1 in aging, dietary restriction, and insulin-like signaling.

How dietary restriction (DR) increases lifespan and decreases disease burden are questions of major interest in biomedical research. Here we report that hypothalamic expression of CREB-binding protein (CBP) and CBP-binding partner Special AT-rich sequence binding protein 1 (SATB-1) is highly correla...

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Autores principales: Minhua Zhang, Michal Poplawski, Kelvin Yen, Hui Cheng, Erik Bloss, Xiao Zhu, Harshil Patel, Charles V Mobbs
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Publicado: Public Library of Science (PLoS) 2009
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spelling oai:doaj.org-article:2d7a20c9f7f94093bc8099468aa80e5d2021-11-25T05:34:29ZRole of CBP and SATB-1 in aging, dietary restriction, and insulin-like signaling.1544-91731545-788510.1371/journal.pbio.1000245https://doaj.org/article/2d7a20c9f7f94093bc8099468aa80e5d2009-11-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19924292/?tool=EBIhttps://doaj.org/toc/1544-9173https://doaj.org/toc/1545-7885How dietary restriction (DR) increases lifespan and decreases disease burden are questions of major interest in biomedical research. Here we report that hypothalamic expression of CREB-binding protein (CBP) and CBP-binding partner Special AT-rich sequence binding protein 1 (SATB-1) is highly correlated with lifespan across five strains of mice, and expression of these genes decreases with age and diabetes in mice. Furthermore, in Caenorhabditis elegans, cbp-1 is induced by bacterial dilution DR (bDR) and the daf-2 mutation, and cbp-1 RNAi specifically in adults completely blocks lifespan extension by three distinct protocols of DR, partially blocks lifespan extension by the daf-2 mutation but not of cold, and blocks delay of other age-related pathologies by bDR. Inhibiting the C. elegans ortholog of SATB-1 and CBP-binding partners daf-16 and hsf-1 also attenuates lifespan extension by bDR, but not other protocols of DR. In a transgenic Abeta42 model of Alzheimer's disease, cbp-1 RNAi prevents protective effects of bDR and accelerates Abeta42-related pathology. Furthermore, consistent with the function of CBP as a histone acetyltransferase, drugs that enhance histone acetylation increase lifespan and reduce Abeta42-related pathology, protective effects completely blocked by cbp-1 RNAi. Other factors implicated in lifespan extension are also CBP-binding partners, suggesting that CBP constitutes a common factor in the modulation of lifespan and disease burden by DR and the insulin/IGF1 signaling pathway.Minhua ZhangMichal PoplawskiKelvin YenHui ChengErik BlossXiao ZhuHarshil PatelCharles V MobbsPublic Library of Science (PLoS)articleBiology (General)QH301-705.5ENPLoS Biology, Vol 7, Iss 11, p e1000245 (2009)
institution DOAJ
collection DOAJ
language EN
topic Biology (General)
QH301-705.5
spellingShingle Biology (General)
QH301-705.5
Minhua Zhang
Michal Poplawski
Kelvin Yen
Hui Cheng
Erik Bloss
Xiao Zhu
Harshil Patel
Charles V Mobbs
Role of CBP and SATB-1 in aging, dietary restriction, and insulin-like signaling.
description How dietary restriction (DR) increases lifespan and decreases disease burden are questions of major interest in biomedical research. Here we report that hypothalamic expression of CREB-binding protein (CBP) and CBP-binding partner Special AT-rich sequence binding protein 1 (SATB-1) is highly correlated with lifespan across five strains of mice, and expression of these genes decreases with age and diabetes in mice. Furthermore, in Caenorhabditis elegans, cbp-1 is induced by bacterial dilution DR (bDR) and the daf-2 mutation, and cbp-1 RNAi specifically in adults completely blocks lifespan extension by three distinct protocols of DR, partially blocks lifespan extension by the daf-2 mutation but not of cold, and blocks delay of other age-related pathologies by bDR. Inhibiting the C. elegans ortholog of SATB-1 and CBP-binding partners daf-16 and hsf-1 also attenuates lifespan extension by bDR, but not other protocols of DR. In a transgenic Abeta42 model of Alzheimer's disease, cbp-1 RNAi prevents protective effects of bDR and accelerates Abeta42-related pathology. Furthermore, consistent with the function of CBP as a histone acetyltransferase, drugs that enhance histone acetylation increase lifespan and reduce Abeta42-related pathology, protective effects completely blocked by cbp-1 RNAi. Other factors implicated in lifespan extension are also CBP-binding partners, suggesting that CBP constitutes a common factor in the modulation of lifespan and disease burden by DR and the insulin/IGF1 signaling pathway.
format article
author Minhua Zhang
Michal Poplawski
Kelvin Yen
Hui Cheng
Erik Bloss
Xiao Zhu
Harshil Patel
Charles V Mobbs
author_facet Minhua Zhang
Michal Poplawski
Kelvin Yen
Hui Cheng
Erik Bloss
Xiao Zhu
Harshil Patel
Charles V Mobbs
author_sort Minhua Zhang
title Role of CBP and SATB-1 in aging, dietary restriction, and insulin-like signaling.
title_short Role of CBP and SATB-1 in aging, dietary restriction, and insulin-like signaling.
title_full Role of CBP and SATB-1 in aging, dietary restriction, and insulin-like signaling.
title_fullStr Role of CBP and SATB-1 in aging, dietary restriction, and insulin-like signaling.
title_full_unstemmed Role of CBP and SATB-1 in aging, dietary restriction, and insulin-like signaling.
title_sort role of cbp and satb-1 in aging, dietary restriction, and insulin-like signaling.
publisher Public Library of Science (PLoS)
publishDate 2009
url https://doaj.org/article/2d7a20c9f7f94093bc8099468aa80e5d
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