Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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 Inner Mitochondrial Membrane01:28

The Inner Mitochondrial Membrane

The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria.  In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The ubiquitin-proteasome system and autophagy as guardians of the cellular proteome.

FEBS letters·2026
Same author

PSG6: A mitochondrially-targeted gentisic acid derivative exerts antiplatelet action via mitochondrial complex I inhibition.

Redox biology·2026
Same author

TBK1 restricts IRGQ-mediated autophagy.

Nature communications·2026
Same author

Intracellular lipopolysaccharide binds RETREG1/FAM134B to regulate ER remodeling upon bacterial infection.

Autophagy·2026
Same author

Discovery and Development of a Potent LIMK2 Isoform-Specific Degrader.

ACS chemical biology·2026
Same author

Corrigendum to "Biglycan evokes autophagy in macrophages via a novel CD44/Toll-like receptor 4 signaling axis in ischemia/reperfusion injury." Kidney International 2019;95:540-562.

Kidney international·2026
Same journal

Addendum: In situ architecture of the human prohibitin complex.

Nature cell biology·2026
Same journal

Evolutionarily conserved short linear motifs drive actin filament binding.

Nature cell biology·2026
Same journal

CD44 restricts EGFR mobility to polarize cytoskeletal signalling modules driving bleb-based migration.

Nature cell biology·2026
Same journal

Author Correction: Mitochondrial fission links ECM mechanotransduction to metabolic redox homeostasis and metastatic chemotherapy resistance.

Nature cell biology·2026
Same journal

An atlas of primate insular cortex reveals a signal-processing strategy in von Economo neurons.

Nature cell biology·2026
Same journal

Primate neurons with special signalling logic.

Nature cell biology·2026
See all related articles

Related Experiment Video

Updated: Jun 16, 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

Mitochondria get a Parkin' ticket.

Philipp Wild1, Ivan Dikic

  • 1Goethe University Medical School, Institute of Biochemistry II and Frankfurt Institute for Molecular Life Sciences, Theodor-Stern-Kai 7, Frankfurt a.M., D-60590, Germany.

Nature Cell Biology
|February 2, 2010
PubMed
Summary
This summary is machine-generated.

Mitochondrial dysfunction is key in Parkinson's disease. The Parkin and PINK1 pathway regulates the removal of damaged mitochondria via autophagy, offering insights into neuroprotection.

More Related Videos

Fluorescence-Based Quantification of Mitochondrial Membrane Potential and Superoxide Levels Using Live Imaging in HeLa Cells
06:57

Fluorescence-Based Quantification of Mitochondrial Membrane Potential and Superoxide Levels Using Live Imaging in HeLa Cells

Published on: May 12, 2023

Related Experiment Videos

Last Updated: Jun 16, 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

Fluorescence-Based Quantification of Mitochondrial Membrane Potential and Superoxide Levels Using Live Imaging in HeLa Cells
06:57

Fluorescence-Based Quantification of Mitochondrial Membrane Potential and Superoxide Levels Using Live Imaging in HeLa Cells

Published on: May 12, 2023

Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • Mitochondrial dysfunction is increasingly recognized as a significant factor in Parkinson's disease pathogenesis.
  • Mutations in the ubiquitin ligase Parkin and the protein kinase PINK1 are directly linked to familial forms of Parkinson's disease.

Purpose of the Study:

  • To elucidate the functional relationship between Parkin, PINK1, and mitochondrial quality control mechanisms in the context of Parkinson's disease.
  • To investigate how the Parkin-PINK1 pathway mediates the selective removal of damaged mitochondria.

Main Methods:

  • Utilizing genetic models and cellular assays to study the Parkin-PINK1 pathway.
  • Investigating the role of ubiquitylation in targeting mitochondria for autophagic degradation.

Main Results:

  • The study highlights the critical role of the Parkin-PINK1 pathway in maintaining mitochondrial health.
  • This pathway links ubiquitylation events on damaged mitochondria to their subsequent clearance through selective autophagy.

Conclusions:

  • The Parkin-PINK1-mediated mitophagy pathway is essential for preventing the accumulation of dysfunctional mitochondria in neurons.
  • Understanding this pathway provides potential therapeutic targets for Parkinson's disease by promoting mitochondrial quality control.