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Related Concept Videos

Mitochondrial Precursor Proteins01:39

Mitochondrial Precursor Proteins

Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
Most of the mitochondrial precursors...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
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,...
The Proteasome01:13

The Proteasome

Eukaryotic cells can degrade proteins through several pathways. One of the most important among these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
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The Proteasome02:18

The Proteasome

Eukaryotic cells can degrade proteins through several pathways. One of the most important amongst these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. A series of enzymes carry out the ubiquitination of the target proteins - E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3...
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,...

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Related Experiment Video

Updated: May 31, 2026

Time-Lapse Video Microscopy for Assessment of EYFP-Parkin Aggregation as a Marker for Cellular Mitophagy
09:29

Time-Lapse Video Microscopy for Assessment of EYFP-Parkin Aggregation as a Marker for Cellular Mitophagy

Published on: May 4, 2016

Preconditioning involves selective mitophagy mediated by Parkin and p62/SQSTM1.

Chengqun Huang1, Allen M Andres, Eric P Ratliff

  • 1The BioScience Center, San Diego State University, San Diego, California, United States of America.

Plos One
|June 21, 2011
PubMed
Summary

Parkin, an E3 ubiquitin ligase, is crucial for mitophagy, the selective removal of damaged mitochondria. This study reveals Parkin and mitophagy are essential for cardioprotection against ischemic injury.

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Time-Lapse Video Microscopy for Assessment of EYFP-Parkin Aggregation as a Marker for Cellular Mitophagy
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Published on: May 4, 2016

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07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

Area of Science:

  • Cellular Biology
  • Cardiovascular Research
  • Mitochondrial Dynamics

Background:

  • Autophagy is vital for cellular homeostasis, particularly in clearing damaged mitochondria.
  • The mechanisms for selective mitochondrial targeting remain unclear.
  • Parkin, an E3 ubiquitin ligase, is implicated in damaged mitochondrial clearance.

Purpose of the Study:

  • Investigate Parkin's role in cardioprotection.
  • Examine Parkin's function in mitophagy during cardiac stress.
  • Determine if Parkin mediates protection offered by ischemic preconditioning (IPC).

Main Methods:

  • Used in vitro simulated ischemia (sI) in HL-1 cells.
  • Employed Langendorff-perfused rat hearts and in vivo mouse models for IPC.
  • Assessed Parkin translocation, mitochondrial elimination, and cell death.
  • Utilized Atg5-deficient cells and p62/SQSTM1 depletion models.
  • Compared wild-type and Parkin knockout mice.

Main Results:

  • Simulated ischemia and IPC induced Parkin translocation to mitochondria.
  • Mitochondrial elimination required autophagy (Atg5-deficient cells).
  • p62/SQSTM1 depletion reduced mitophagy and increased cell death.
  • Parkin knockout mice showed blunted IPC-induced p62 translocation and lost cardioprotection.

Conclusions:

  • Parkin is essential for Parkin-mediated mitophagy in cardiomyocytes.
  • Parkin and mitophagy are critical for cardioprotection induced by IPC.
  • This study elucidates a novel mechanism of cardiac protection involving Parkin and mitophagy.