AMPK: A key sensor of fuel and energy status in skeletal muscle

Research output: Contribution to journal › Review › Research › peer-review

Standard

AMPK : A key sensor of fuel and energy status in skeletal muscle. / Hardie, D. Grahame; Sakamoto, Kei.

In: Physiology, Vol. 21, No. 1, 01.02.2006, p. 48-60.

Research output: Contribution to journal › Review › Research › peer-review

Harvard

Hardie, DG & Sakamoto, K 2006, 'AMPK: A key sensor of fuel and energy status in skeletal muscle', Physiology, vol. 21, no. 1, pp. 48-60. https://doi.org/10.1152/physiol.00044.2005

APA

Hardie, D. G., & Sakamoto, K. (2006). AMPK: A key sensor of fuel and energy status in skeletal muscle. Physiology, 21(1), 48-60. https://doi.org/10.1152/physiol.00044.2005

Vancouver

Hardie DG, Sakamoto K. AMPK: A key sensor of fuel and energy status in skeletal muscle. Physiology. 2006 Feb 1;21(1):48-60. https://doi.org/10.1152/physiol.00044.2005

Author

Hardie, D. Grahame ; Sakamoto, Kei. / AMPK : A key sensor of fuel and energy status in skeletal muscle. In: Physiology. 2006 ; Vol. 21, No. 1. pp. 48-60.

Bibtex

@article{fa174a7afcb6472e830af5f6e877e2aa,
title = "AMPK: A key sensor of fuel and energy status in skeletal muscle",
abstract = "Contraction induces marked metabolic changes in muscle, and the AMP-activated protein kinase (AMPK) is a good candidate to explain these effects. Recent work using a muscle-specific knockout of the upstream kinase, LKB1, has confirmed that the LKB1→AMPK cascade is the signaling pathway responsible for many of these effects.",
author = "Hardie, {D. Grahame} and Kei Sakamoto",
year = "2006",
month = feb,
day = "1",
doi = "10.1152/physiol.00044.2005",
language = "English",
volume = "21",
pages = "48--60",
journal = "Physiology",
issn = "1548-9213",
publisher = "American Physiological Society",
number = "1",

}

RIS

TY - JOUR

T1 - AMPK

T2 - A key sensor of fuel and energy status in skeletal muscle

AU - Hardie, D. Grahame

AU - Sakamoto, Kei

PY - 2006/2/1

Y1 - 2006/2/1

N2 - Contraction induces marked metabolic changes in muscle, and the AMP-activated protein kinase (AMPK) is a good candidate to explain these effects. Recent work using a muscle-specific knockout of the upstream kinase, LKB1, has confirmed that the LKB1→AMPK cascade is the signaling pathway responsible for many of these effects.

AB - Contraction induces marked metabolic changes in muscle, and the AMP-activated protein kinase (AMPK) is a good candidate to explain these effects. Recent work using a muscle-specific knockout of the upstream kinase, LKB1, has confirmed that the LKB1→AMPK cascade is the signaling pathway responsible for many of these effects.

UR - http://www.scopus.com/inward/record.url?scp=33644943620&partnerID=8YFLogxK

U2 - 10.1152/physiol.00044.2005

DO - 10.1152/physiol.00044.2005

M3 - Review

C2 - 16443822

AN - SCOPUS:33644943620

VL - 21

SP - 48

EP - 60

JO - Physiology

JF - Physiology

SN - 1548-9213

IS - 1

ER -

ID: 239585457