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Related Concept Videos

Autophagy01:27

Autophagy

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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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PI3K/mTOR/AKT Signaling Pathway01:22

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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Autophagic Cell Death01:18

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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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Delivery Pathways to the Lysosome01:36

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Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
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mTOR Signaling and Cancer Progression03:03

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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cAMP-dependent Protein Kinase Pathways01:25

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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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Study of Protein-protein Interactions in Autophagy Research
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AMPK and Autophagy.

Yanjun Li1, Yingyu Chen2

  • 1College of Life Sciences, Nankai University, Tianjin, China.

Advances in Experimental Medicine and Biology
|November 29, 2019
PubMed
Summary
This summary is machine-generated.

AMPK, a cellular energy sensor, activates autophagy and mitophagy by regulating key proteins and genes. This process is crucial for cellular metabolism and response to energy levels.

Keywords:
AMPKAutophagyMitophagy

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Area of Science:

  • Cellular Biology
  • Metabolism
  • Biochemistry

Background:

  • AMPK (AMP-activated protein kinase) is a critical cellular energy sensor.
  • It regulates metabolic pathways by sensing cellular ATP levels.
  • AMPK activation influences both catabolic and anabolic processes.

Purpose of the Study:

  • To detail the molecular structure of AMPK.
  • To explain the regulatory mechanisms of AMPK activity.
  • To elucidate AMPK's role in regulating autophagy and mitophagy.

Main Methods:

  • Review of molecular mechanisms of AMPK activation.
  • Analysis of AMPK's direct and indirect regulation of autophagy pathways.
  • Examination of AMPK's role in mitophagy initiation.

Main Results:

  • AMPK activation, triggered by AMP/ADP binding, upregulates catabolism and inhibits anabolism.
  • AMPK directly phosphorylates key autophagy-related proteins in mTORC1, ULK1, and PIK3C3/VPS34 complexes.
  • AMPK indirectly controls autophagy gene expression via transcription factors like FOXO3, TFEB, and BRD4.
  • AMPK promotes mitophagy by inducing mitochondrial fragmentation and recruiting autophagy machinery.

Conclusions:

  • AMPK plays a pivotal role in cellular energy homeostasis through autophagy and mitophagy.
  • Understanding AMPK regulation provides insights into metabolic disease.
  • Targeting AMPK may offer therapeutic strategies for metabolic disorders.