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The SKN-1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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The SKN-1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms. / Tullet, Jennifer M.a.; Green, James W.; Au, Catherine et al.
In: Aging Cell, Vol. 16, No. 5, 10.2017, p. 1191-1194.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Tullet, JMA, Green, JW, Au, C, Benedetto, A, Thompson, MA, Clark, E, Gilliat, AF, Young, A, Schmeisser, K & Gems, D 2017, 'The SKN-1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms', Aging Cell, vol. 16, no. 5, pp. 1191-1194. https://doi.org/10.1111/acel.12627

APA

Tullet, J. M. A., Green, J. W., Au, C., Benedetto, A., Thompson, M. A., Clark, E., Gilliat, A. F., Young, A., Schmeisser, K., & Gems, D. (2017). The SKN-1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms. Aging Cell, 16(5), 1191-1194. https://doi.org/10.1111/acel.12627

Vancouver

Tullet JMA, Green JW, Au C, Benedetto A, Thompson MA, Clark E et al. The SKN-1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms. Aging Cell. 2017 Oct;16(5):1191-1194. Epub 2017 Jun 14. doi: 10.1111/acel.12627

Author

Tullet, Jennifer M.a. ; Green, James W. ; Au, Catherine et al. / The SKN-1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms. In: Aging Cell. 2017 ; Vol. 16, No. 5. pp. 1191-1194.

Bibtex

@article{b250d2b9b4c84717acd76b991792de76,
title = "The SKN-1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms",
abstract = "In C. elegans, the skn-1 gene encodes a transcription factor that resembles mammalian Nrf2 and activates a detoxification response. skn-1 promotes resistance to oxidative stress (Oxr) and also increases lifespan, and it has been suggested that the former causes the latter, consistent with the theory that oxidative damage causes aging. Here, we report that effects of SKN-1 on Oxr and longevity can be dissociated. We also establish that skn-1 expression can be activated by the DAF-16/FoxO transcription factor, another central regulator of growth, metabolism, and aging. Notably, skn-1 is required for Oxr but not increased lifespan resulting from over-expression of DAF-16; concomitantly, DAF-16 over-expression rescues the short lifespan of skn-1 mutants but not their hypersensitivity to oxidative stress. These results suggest that SKN-1 promotes longevity by a mechanism other than protection against oxidative damage.",
author = "Tullet, {Jennifer M.a.} and Green, {James W.} and Catherine Au and Alexandre Benedetto and Thompson, {Maximillian A.} and Emily Clark and Gilliat, {Ann F.} and Adelaide Young and Kathrin Schmeisser and David Gems",
year = "2017",
month = oct,
doi = "10.1111/acel.12627",
language = "English",
volume = "16",
pages = "1191--1194",
journal = "Aging Cell",
issn = "1474-9718",
publisher = "Wiley-Blackwell",
number = "5",

}

RIS

TY - JOUR

T1 - The SKN-1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms

AU - Tullet, Jennifer M.a.

AU - Green, James W.

AU - Au, Catherine

AU - Benedetto, Alexandre

AU - Thompson, Maximillian A.

AU - Clark, Emily

AU - Gilliat, Ann F.

AU - Young, Adelaide

AU - Schmeisser, Kathrin

AU - Gems, David

PY - 2017/10

Y1 - 2017/10

N2 - In C. elegans, the skn-1 gene encodes a transcription factor that resembles mammalian Nrf2 and activates a detoxification response. skn-1 promotes resistance to oxidative stress (Oxr) and also increases lifespan, and it has been suggested that the former causes the latter, consistent with the theory that oxidative damage causes aging. Here, we report that effects of SKN-1 on Oxr and longevity can be dissociated. We also establish that skn-1 expression can be activated by the DAF-16/FoxO transcription factor, another central regulator of growth, metabolism, and aging. Notably, skn-1 is required for Oxr but not increased lifespan resulting from over-expression of DAF-16; concomitantly, DAF-16 over-expression rescues the short lifespan of skn-1 mutants but not their hypersensitivity to oxidative stress. These results suggest that SKN-1 promotes longevity by a mechanism other than protection against oxidative damage.

AB - In C. elegans, the skn-1 gene encodes a transcription factor that resembles mammalian Nrf2 and activates a detoxification response. skn-1 promotes resistance to oxidative stress (Oxr) and also increases lifespan, and it has been suggested that the former causes the latter, consistent with the theory that oxidative damage causes aging. Here, we report that effects of SKN-1 on Oxr and longevity can be dissociated. We also establish that skn-1 expression can be activated by the DAF-16/FoxO transcription factor, another central regulator of growth, metabolism, and aging. Notably, skn-1 is required for Oxr but not increased lifespan resulting from over-expression of DAF-16; concomitantly, DAF-16 over-expression rescues the short lifespan of skn-1 mutants but not their hypersensitivity to oxidative stress. These results suggest that SKN-1 promotes longevity by a mechanism other than protection against oxidative damage.

U2 - 10.1111/acel.12627

DO - 10.1111/acel.12627

M3 - Journal article

VL - 16

SP - 1191

EP - 1194

JO - Aging Cell

JF - Aging Cell

SN - 1474-9718

IS - 5

ER -