Nutrient-dependent acetylation controls basic regulatory metabolic switches and cellular reprogramming

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Nutrient-dependent acetylation controls basic regulatory metabolic switches and cellular reprogramming. / Dominy, J. E.; Gerhart-Hines, Z.; Puigserver, P.

In: Cold Spring Harbor Symposia on Quantitative Biology, Vol. 76, 2011, p. 203-209.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Dominy, JE, Gerhart-Hines, Z & Puigserver, P 2011, 'Nutrient-dependent acetylation controls basic regulatory metabolic switches and cellular reprogramming', Cold Spring Harbor Symposia on Quantitative Biology, vol. 76, pp. 203-209. https://doi.org/10.1101/sqb.2012.76.010843

APA

Dominy, J. E., Gerhart-Hines, Z., & Puigserver, P. (2011). Nutrient-dependent acetylation controls basic regulatory metabolic switches and cellular reprogramming. Cold Spring Harbor Symposia on Quantitative Biology, 76, 203-209. https://doi.org/10.1101/sqb.2012.76.010843

Vancouver

Dominy JE, Gerhart-Hines Z, Puigserver P. Nutrient-dependent acetylation controls basic regulatory metabolic switches and cellular reprogramming. Cold Spring Harbor Symposia on Quantitative Biology. 2011;76:203-209. https://doi.org/10.1101/sqb.2012.76.010843

Author

Dominy, J. E. ; Gerhart-Hines, Z. ; Puigserver, P. / Nutrient-dependent acetylation controls basic regulatory metabolic switches and cellular reprogramming. In: Cold Spring Harbor Symposia on Quantitative Biology. 2011 ; Vol. 76. pp. 203-209.

Bibtex

@article{73b88eece1b3499db23718ffc39f375b,
title = "Nutrient-dependent acetylation controls basic regulatory metabolic switches and cellular reprogramming",
abstract = "Organisms must be able to selectively tailor their ability to use the macronutrients of carbohydrate, protein, and fat based on their availability. In different cell types, how the nutrient fluctuations are sensed and the mechanisms by which the pathways of central metabolism are switched to favor the use of one particular nutrient type over another are topics of intense interest. Protein acetylation is one major evolutionary conserved mechanism by which nutrient fluctuations are sensed within cells and subsequently coupled with metabolic switching. In this review, we present the case of PGC-1α acetylation and how the control of PGC-1α's activity by acetylation sets into motion a wide range of metabolic adaptations that makes this protein an exemplary model for acetylation-mediated mechanisms of nutrient sensing and communication.",
author = "Dominy, {J. E.} and Z. Gerhart-Hines and P. Puigserver",
year = "2011",
doi = "10.1101/sqb.2012.76.010843",
language = "English",
volume = "76",
pages = "203--209",
journal = "Cold Spring Harbor Laboratory. Symposia on Quantitative Biology",
issn = "0091-7451",
publisher = "Cold Spring Harbor Laboratory Press",

}

RIS

TY - JOUR

T1 - Nutrient-dependent acetylation controls basic regulatory metabolic switches and cellular reprogramming

AU - Dominy, J. E.

AU - Gerhart-Hines, Z.

AU - Puigserver, P.

PY - 2011

Y1 - 2011

N2 - Organisms must be able to selectively tailor their ability to use the macronutrients of carbohydrate, protein, and fat based on their availability. In different cell types, how the nutrient fluctuations are sensed and the mechanisms by which the pathways of central metabolism are switched to favor the use of one particular nutrient type over another are topics of intense interest. Protein acetylation is one major evolutionary conserved mechanism by which nutrient fluctuations are sensed within cells and subsequently coupled with metabolic switching. In this review, we present the case of PGC-1α acetylation and how the control of PGC-1α's activity by acetylation sets into motion a wide range of metabolic adaptations that makes this protein an exemplary model for acetylation-mediated mechanisms of nutrient sensing and communication.

AB - Organisms must be able to selectively tailor their ability to use the macronutrients of carbohydrate, protein, and fat based on their availability. In different cell types, how the nutrient fluctuations are sensed and the mechanisms by which the pathways of central metabolism are switched to favor the use of one particular nutrient type over another are topics of intense interest. Protein acetylation is one major evolutionary conserved mechanism by which nutrient fluctuations are sensed within cells and subsequently coupled with metabolic switching. In this review, we present the case of PGC-1α acetylation and how the control of PGC-1α's activity by acetylation sets into motion a wide range of metabolic adaptations that makes this protein an exemplary model for acetylation-mediated mechanisms of nutrient sensing and communication.

UR - http://www.scopus.com/inward/record.url?scp=84867414867&partnerID=8YFLogxK

U2 - 10.1101/sqb.2012.76.010843

DO - 10.1101/sqb.2012.76.010843

M3 - Journal article

C2 - 22371372

AN - SCOPUS:84867414867

VL - 76

SP - 203

EP - 209

JO - Cold Spring Harbor Laboratory. Symposia on Quantitative Biology

JF - Cold Spring Harbor Laboratory. Symposia on Quantitative Biology

SN - 0091-7451

ER -

ID: 347796196