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AMPK Activates ULK1 in Skeletal Muscle Without Increasing Markers of Autophagy.

Record Type:	Language materials, manuscript : Monograph/item
Title/Author:	AMPK Activates ULK1 in Skeletal Muscle Without Increasing Markers of Autophagy./
Author:	Hagen, Margaret T.
Description:	1 online resource (60 pages)
Notes:	Source: Masters Abstracts International, Volume: 83-02.
Contained By:	Masters Abstracts International83-02.
Subject:	Molecular biology. -
Online resource:	click for full text (PQDT)
ISBN:	9798534667776

AMPK Activates ULK1 in Skeletal Muscle Without Increasing Markers of Autophagy.
Hagen, Margaret T.

AMPK Activates ULK1 in Skeletal Muscle Without Increasing Markers of Autophagy. - 1 online resource (60 pages)

Source: Masters Abstracts International, Volume: 83-02.

Thesis (M.S.)--Saint Louis University, 2021.

Includes bibliographical references

Metabolic disorders and aging diseases impact a large portion of the population. Exercise, and the metabolic stress that it causes in cells, has been shown to have many positive effects in preventing and reducing the impacts of these conditions, in part through the engagement of autophagy, a regulated pathway for degradation of intracellular contents, and modulation of glucose metabolism. We tested the effects of an exercise mimetic, 5-aminoimidazole-4-carboxamide riboside (AICAR), to see what effects it would have on some of the pathways proposed to be responsible for these benefits. We hypothesized that AICAR would cause an increase in levels of autophagy and glucose metabolism through the phosphorylation of Unc51 like kinase (ULK1) and its interaction with downstream proteins. We looked at autophagy related protein 14 (ATG14) for general autophagy, hexokinase (HK) and phosphofructokinase (PFK) activity for the pentose phosphate pathway (PPP) and glycolysis respectively, and both the GTPase ras-related protein-receptor interacting protein 1-dynamin-related protein 1 (RAB9-RIP1-DRP1) pathway and the PTEN-induced kinase 1-Parkin1 (PINK1-Parkin) pathways for mitophagy. We utilized C2C12 myoblasts, a mouse cell line, and satellite cells harvested directly from mouse hindlimbs, and observed the impacts of AICAR and transfected versions of ULK1 with various levels of inhibited function. Western blot analysis of protein phosphorylation levels showed an increase in 5' AMP activated protein kinase (AMPK), and ULK1 levels following AICAR exposure, but no rise in the activation of proteins in the autophagy or mitophagy pathways we looked at downstream of ULK1. Surprisingly, the only significant changes we found were a decrease in ATG14 phosphorylation and PINK1 expression in the cells with AICAR exposure; the other pathways showed no change. These results suggest that activation of AMPK and ULK1 by AICAR is insufficient to induce autophagy or mitophagy, indicating that if exercise does induce autophagy in skeletal muscle, some other aspect in addition to AMPK/ULK1 activation is required for its initiation.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024

Mode of access: World Wide Web

ISBN: 9798534667776Subjects--Topical Terms:

583443
Molecular biology.
Subjects--Index Terms:

5-Aminoimidazole-4-carboxamide ribonucleotideIndex Terms--Genre/Form:

554714
Electronic books.

AMPK Activates ULK1 in Skeletal Muscle Without Increasing Markers of Autophagy.
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