ampk and mtor regulate autophagy through direct phosphorylation of ulk1 pdf Sunday, May 23, 2021 5:46:51 PM

Ampk And Mtor Regulate Autophagy Through Direct Phosphorylation Of Ulk1 Pdf

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Protein Phosphorylation in Human Health. Macroautophagy hereafter called autophagy is an intracellular lysosomal degradation process. Long-lived cytosolic proteins and entire organelles are enveloped by a double membrane.

The Role of AMPK Activation for Cardioprotection in Doxorubicin-Induced Cardiotoxicity

Review Free access Phone: Find articles by Kim, Y. Find articles by Guan, K. Published January 2, - More info. Nutrients, growth factors, and cellular energy levels are key determinants of cell growth and proliferation.

Autophagy is an intracellular degradation pathway targeting organelles and macromolecules, thereby regulating various cellular functions. Phosphorylation is a key posttranscriptional protein modification implicated in the regulation of biological function including autophagy. Under asynchronous conditions, autophagy activity is predominantly suppressed by mechanistic target of rapamycin mTOR kinase, but whether autophagy-related genes ATG proteins are phosphorylated differentially throughout the sequential phases of the cell cycle remains unclear. This phosphorylation induces autophagy and, surprisingly, is shown to drive cell cycle progression. This work reveals a yet-unappreciated role for autophagy in cell cycle progression and enhances our understanding of the specific phase-dependent autophagy regulation during cellular growth and proliferation. PLoS Biol 18 6 : e This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Regulation of Autophagy by Protein Phosphorylation

Doxorubicin is a commonly used chemotherapeutic agent for the treatment of a range of cancers, but despite its success in improving cancer survival rates, doxorubicin is cardiotoxic and can lead to congestive heart failure. Therapeutic options for this patient group are limited to standard heart failure medications with the only drug specific for doxorubicin cardiotoxicity to reach FDA approval being dexrazoxane, an iron-chelating agent targeting oxidative stress. However, dexrazoxane has failed to live up to its expectations from preclinical studies while also bringing up concerns about its safety. Despite decades of research, the molecular mechanisms of doxorubicin cardiotoxicity are still poorly understood and oxidative stress is no longer considered to be the sole evil. Mitochondrial impairment, increased apoptosis, dysregulated autophagy and increased fibrosis have also been shown to be crucial players in doxorubicin cardiotoxicity. These cellular processes are all linked by one highly conserved intracellular kinase: adenosine monophosphate—activated protein kinase AMPK.

Regulation of Autophagy by Protein Phosphorylation

This is an open access article distributed under the terms of Creative Commons Attribution License. Age-related hearing loss ARHL , also known as presbycusis, is a complex degenerative disease characterized by declining auditory function, including increased hearing thresholds and reduced frequency resolution 1. ARHL is one of the most prevalent and chronic conditions of older populations, affecting tens of millions of people worldwide 2 , and may cause social isolation, depression, and even dementia 3. In addition to degeneration of the peripheral auditory organs, auditory cortex degeneration has been demonstrated to serve a crucial role in ARHL pathogenesis 4 , 5 ; however, the molecular mechanism is not well understood. D-galactose D-gal is a reducing sugar and is oxidized into aldehydes and H 2 O 2 when present at high levels 6.

Cardiac troponin I cTnI , and transmission electron microscopy TEM , along with hematoxylin-basic fuchsin-picric acid HBFP staining, were used to evaluate the myocardial ischemic-hypoxic injury and protection. Western blot was used to analyze the relationship of autophagy-associated proteins. Exhaustive exercise caused severe myocardial ischemic-hypoxic injury, which led to an increase in cTnI levels, changes of ischemia—hypoxia, and cells ultrastructure.

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mTOR: a pharmacologic target for autophagy regulation

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AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1

1 Comments

Dovisabooks 24.05.2021 at 12:00

Under glucose starvation, AMPK promotes autophagy by directly activating Ulk1 through phosphorylation of Ser and Ser Under nutrient.

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