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Related Concept Videos

Autophagy01:27

Autophagy

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.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

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.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Autophagic Cell Death01:18

Autophagic Cell Death

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.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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.
The mTOR pathway or the...

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Related Experiment Video

Updated: Jun 3, 2026

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome
07:56

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Published on: November 30, 2022

Mitochondria regulate autophagy by conserved signalling pathways.

Martin Graef1, Jodi Nunnari

  • 1Department of Molecular and Cellular Biology, Davis University of California, Davis, CA, USA.

The EMBO Journal
|April 7, 2011
PubMed
Summary
This summary is machine-generated.

Mitochondrial dysfunction impairs cellular quality control by inhibiting autophagy, a key process for maintaining cell health. This link between mitochondrial health and autophagy is crucial for understanding aging and neurodegenerative diseases.

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In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice
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Sensitive Measurement of Mitophagy by Flow Cytometry Using the pH-dependent Fluorescent Reporter mt-Keima
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Sensitive Measurement of Mitophagy by Flow Cytometry Using the pH-dependent Fluorescent Reporter mt-Keima

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Related Experiment Videos

Last Updated: Jun 3, 2026

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome
07:56

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Published on: November 30, 2022

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08:40

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice

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09:13

Sensitive Measurement of Mitophagy by Flow Cytometry Using the pH-dependent Fluorescent Reporter mt-Keima

Published on: August 12, 2018

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Autophagy is a vital cellular process for homeostasis and quality control, involving the degradation of cellular components like mitochondria.
  • Mitochondrial dysfunction is implicated in various age-related diseases.

Purpose of the Study:

  • To investigate the regulatory link between mitochondrial function and autophagy in Saccharomyces cerevisiae.
  • To elucidate the roles of specific protein kinases in mediating this relationship.

Main Methods:

  • Analysis of autophagic response during amino-acid starvation in yeast models.
  • Investigating the impact of mitochondrial respiratory deficiency on autophagy.
  • Assessing the activity of protein kinases Atg1, TORC1, and PKA.

Main Results:

  • Mitochondrial respiratory deficiency significantly compromises both autophagy gene induction and autophagic flux.
  • Protein kinases Atg1, TORC1, and PKA regulate autophagic flux, while PKA alone controls autophagy gene induction.
  • Mitochondrial dysfunction suppresses autophagic flux and gene induction by stimulating PKA activity, inhibiting Atg1-Atg13 complex recruitment.

Conclusions:

  • A direct regulatory link exists between mitochondrial function and autophagy.
  • Mitochondrial dysfunction and autophagy inhibition are interconnected risk factors for aging, cancerogenesis, and neurodegeneration.