AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle

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Standard

AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle. / Li, Jingwen; Knudsen, Jonas Roland; Henriquez-Olguin, Carlos; Li, Zhencheng; Birk, Jesper Bratz; Persson, Kaspar W; Hellsten, Ylva; Offergeld, Anika; Jarassier, William; Grand, Fabien L; Schjerling, Peter; Wojtaszewski, Jørgen; Jensen, Thomas Elbenhardt.

I: Journal of Physiology, Bind 599, Nr. 12, 2021, s. 3081-3100.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Li, J, Knudsen, JR, Henriquez-Olguin, C, Li, Z, Birk, JB, Persson, KW, Hellsten, Y, Offergeld, A, Jarassier, W, Grand, FL, Schjerling, P, Wojtaszewski, J & Jensen, TE 2021, 'AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle', Journal of Physiology, bind 599, nr. 12, s. 3081-3100. https://doi.org/10.1113/JP281187

APA

Li, J., Knudsen, J. R., Henriquez-Olguin, C., Li, Z., Birk, J. B., Persson, K. W., Hellsten, Y., Offergeld, A., Jarassier, W., Grand, F. L., Schjerling, P., Wojtaszewski, J., & Jensen, T. E. (2021). AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle. Journal of Physiology, 599(12), 3081-3100. https://doi.org/10.1113/JP281187

Vancouver

Li J, Knudsen JR, Henriquez-Olguin C, Li Z, Birk JB, Persson KW o.a. AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle. Journal of Physiology. 2021;599(12):3081-3100. https://doi.org/10.1113/JP281187

Author

Li, Jingwen ; Knudsen, Jonas Roland ; Henriquez-Olguin, Carlos ; Li, Zhencheng ; Birk, Jesper Bratz ; Persson, Kaspar W ; Hellsten, Ylva ; Offergeld, Anika ; Jarassier, William ; Grand, Fabien L ; Schjerling, Peter ; Wojtaszewski, Jørgen ; Jensen, Thomas Elbenhardt. / AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle. I: Journal of Physiology. 2021 ; Bind 599, Nr. 12. s. 3081-3100.

Bibtex

@article{36a6210d621047d399c1249b0e9bdde7,
title = "AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle",
abstract = "AXIN1 is a scaffold protein known to interact with >20 proteins in signal transduction pathways regulating cellular development and function. Recently, AXIN1 was proposed to assemble a protein complex essential to catabolic-anabolic transition by coordinating AMPK activation and inactivation of mTORC1 and to regulate glucose uptake-stimulation by both AMPK and insulin. To investigate whether AXIN1 is permissive for adult skeletal muscle function, a phenotypic in vivo and ex vivo characterization of tamoxifen-inducible skeletal muscle-specific AXIN1 knockout (AXIN1 imKO) mice was conducted. AXIN1 imKO did not influence AMPK/mTORC1 signaling or glucose uptake stimulation, neither at rest nor in response to different exercise/contraction protocols, pharmacological AMPK activation, insulin or amino acids stimulation. The only genotypic difference observed was in exercising gastrocnemius muscle, where AXIN1 imKO displayed elevated α2/β2/γ3 AMPK activity and AMP/ATP ratio compared to wild-type mice. Our work shows that AXIN1 imKO generally does not affect skeletal muscle AMPK/mTORC1 signaling and glucose metabolism, likely due to functional redundancy of its homolog AXIN2. ",
author = "Jingwen Li and Knudsen, {Jonas Roland} and Carlos Henriquez-Olguin and Zhencheng Li and Birk, {Jesper Bratz} and Persson, {Kaspar W} and Ylva Hellsten and Anika Offergeld and William Jarassier and Grand, {Fabien L} and Peter Schjerling and J{\o}rgen Wojtaszewski and Jensen, {Thomas Elbenhardt}",
note = "This article is protected by copyright. All rights reserved.",
year = "2021",
doi = "10.1113/JP281187",
language = "English",
volume = "599",
pages = "3081--3100",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "12",

}

RIS

TY - JOUR

T1 - AXIN1 knockout does not alter AMPK/mTORC1 regulation and glucose metabolism in mouse skeletal muscle

AU - Li, Jingwen

AU - Knudsen, Jonas Roland

AU - Henriquez-Olguin, Carlos

AU - Li, Zhencheng

AU - Birk, Jesper Bratz

AU - Persson, Kaspar W

AU - Hellsten, Ylva

AU - Offergeld, Anika

AU - Jarassier, William

AU - Grand, Fabien L

AU - Schjerling, Peter

AU - Wojtaszewski, Jørgen

AU - Jensen, Thomas Elbenhardt

N1 - This article is protected by copyright. All rights reserved.

PY - 2021

Y1 - 2021

N2 - AXIN1 is a scaffold protein known to interact with >20 proteins in signal transduction pathways regulating cellular development and function. Recently, AXIN1 was proposed to assemble a protein complex essential to catabolic-anabolic transition by coordinating AMPK activation and inactivation of mTORC1 and to regulate glucose uptake-stimulation by both AMPK and insulin. To investigate whether AXIN1 is permissive for adult skeletal muscle function, a phenotypic in vivo and ex vivo characterization of tamoxifen-inducible skeletal muscle-specific AXIN1 knockout (AXIN1 imKO) mice was conducted. AXIN1 imKO did not influence AMPK/mTORC1 signaling or glucose uptake stimulation, neither at rest nor in response to different exercise/contraction protocols, pharmacological AMPK activation, insulin or amino acids stimulation. The only genotypic difference observed was in exercising gastrocnemius muscle, where AXIN1 imKO displayed elevated α2/β2/γ3 AMPK activity and AMP/ATP ratio compared to wild-type mice. Our work shows that AXIN1 imKO generally does not affect skeletal muscle AMPK/mTORC1 signaling and glucose metabolism, likely due to functional redundancy of its homolog AXIN2. 

AB - AXIN1 is a scaffold protein known to interact with >20 proteins in signal transduction pathways regulating cellular development and function. Recently, AXIN1 was proposed to assemble a protein complex essential to catabolic-anabolic transition by coordinating AMPK activation and inactivation of mTORC1 and to regulate glucose uptake-stimulation by both AMPK and insulin. To investigate whether AXIN1 is permissive for adult skeletal muscle function, a phenotypic in vivo and ex vivo characterization of tamoxifen-inducible skeletal muscle-specific AXIN1 knockout (AXIN1 imKO) mice was conducted. AXIN1 imKO did not influence AMPK/mTORC1 signaling or glucose uptake stimulation, neither at rest nor in response to different exercise/contraction protocols, pharmacological AMPK activation, insulin or amino acids stimulation. The only genotypic difference observed was in exercising gastrocnemius muscle, where AXIN1 imKO displayed elevated α2/β2/γ3 AMPK activity and AMP/ATP ratio compared to wild-type mice. Our work shows that AXIN1 imKO generally does not affect skeletal muscle AMPK/mTORC1 signaling and glucose metabolism, likely due to functional redundancy of its homolog AXIN2. 

U2 - 10.1113/JP281187

DO - 10.1113/JP281187

M3 - Journal article

C2 - 33913171

VL - 599

SP - 3081

EP - 3100

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 12

ER -

ID: 260992560