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

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

You might also read

Related Articles

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

Sort by
Same author

Identification of key metabolic enzymes involved in the activation of obeldesivir and remdesivir to the active triphosphate metabolite.

Antimicrobial agents and chemotherapy·2026
Same author

Correction: Sooreshjani et al. LIMK2-NKX3.1 Engagement Promotes Castration-Resistant Prostate Cancer. <i>Cancers</i> 2021, <i>13</i>, 2324.

Cancers·2026
Same author

High throughput, automated and fully contained cytokine release assay using primary human CD4<sup>+</sup> T cells.

SLAS discovery : advancing life sciences R & D·2026
Same author

Cadmium-drought interaction modulates oxidative stress, antioxidant defense, and stress-responsive gene in rice sprouts.

Physiology and molecular biology of plants : an international journal of functional plant biology·2026
Same author

Spatial transcriptional profiling of CHB liver biopsies reveals an undetected population of zonally biased HBV-integrated cells.

JHEP reports : innovation in hepatology·2026
Same author

Discovery of an ITK and TRK kinase inhibitor for the potential topical treatment of atopic dermatitis.

Nature communications·2026

Related Experiment Video

Updated: Jul 2, 2026

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
13:15

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1

Published on: February 25, 2016

Deregulated Cdk5 promotes oxidative stress and mitochondrial dysfunction.

Kai-Hui Sun1, Yolanda de Pablo, Fabien Vincent

  • 1Department of Chemistry and Purdue Cancer Center, Purdue University, West Lafayette, IN 47907, USA.

Journal of Neurochemistry
|August 12, 2008
PubMed
Summary

Cyclin-dependent kinase 5 (Cdk5) dysregulation causes oxidative stress and mitochondrial damage in early Alzheimer's disease (AD). Inhibiting Cdk5 protects against neurodegeneration and cell death, suggesting Cdk5 as a therapeutic target for AD.

More Related Videos

Ratiometric Biosensors that Measure Mitochondrial Redox State and ATP in Living Yeast Cells
12:22

Ratiometric Biosensors that Measure Mitochondrial Redox State and ATP in Living Yeast Cells

Published on: July 22, 2013

Related Experiment Videos

Last Updated: Jul 2, 2026

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
13:15

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1

Published on: February 25, 2016

Ratiometric Biosensors that Measure Mitochondrial Redox State and ATP in Living Yeast Cells
12:22

Ratiometric Biosensors that Measure Mitochondrial Redox State and ATP in Living Yeast Cells

Published on: July 22, 2013

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Oxidative stress is an early indicator of Alzheimer's disease (AD).
  • Deregulation of cyclin-dependent kinase 5 (Cdk5) has been implicated in compromising cellular antioxidant defenses.

Purpose of the Study:

  • To elucidate the mechanism by which Cdk5 contributes to oxidative stress and neuronal cell death in AD.
  • To investigate the potential of Cdk5 modulators as a therapeutic strategy for AD.

Main Methods:

  • Utilized novel Cdk5 modulators to study Cdk5's role in oxidative stress.
  • Assessed the impact of Cdk5 dysregulation on reactive oxygen species (ROS) levels and mitochondrial function.
  • Investigated the feedback loop involving Cdk5, ROS, and mitochondrial damage in AD pathogenesis.

Main Results:

  • Cdk5 dysregulation leads to ROS accumulation via inactivation of peroxiredoxin I and II.
  • Cdk5 inhibition mitigates mitochondrial damage and rescues neuronal cells from neurotoxic insults.
  • A positive feedback loop between Cdk5, ROS, and mitochondrial dysfunction contributes to cell death in late-stage AD.

Conclusions:

  • Cdk5 is an upstream regulator of mitochondrial dysfunction and oxidative stress in AD.
  • Targeting Cdk5 offers a promising therapeutic avenue for preventing neurodegeneration in Alzheimer's disease.