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

Drugs that Stabilize Microtubules01:15

Drugs that Stabilize Microtubules

2.0K
Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
2.0K
Intralumenal Vesicles and Multivesicular Bodies01:38

Intralumenal Vesicles and Multivesicular Bodies

3.5K
Intraluminal vesicles (ILVs) are small vesicles 50-80 nm in diameter formed during the maturation of early endosomes. A specialized endosome containing numerous ILVs is called a multivesicular body (MVB). ILVs contain internalized molecules such as antigens, nucleic acids, proteins, and metabolites. Some of these molecules are released from the MVBs inside exosomes and are transported to other cells. Other MVBs contain molecules that are retained in the ILVs and are later degraded within the...
3.5K
Drugs that Destabilize Microtubules01:10

Drugs that Destabilize Microtubules

2.0K
Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
2.0K

You might also read

Related Articles

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

Sort by
Same author

Influence of Joint Structure in Multibody Model on Behavior Analysis of Crash Test Dummy.

Stapp car crash journal·2026
Same author

GAK antagonises ROCK-dependent regulation of actomyosin dynamics.

Journal of cell science·2026
Same author

Myeloid-specific Exoc5 deficiency develops renal inflammation and hypertension.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2026
Same author

[Rectosigmoid Colon Cancer with Unresectable Liver Metastases That Responded Remarkably to Bevacizumab-Combined Chemotherapy-A Case Report].

Gan to kagaku ryoho. Cancer & chemotherapy·2025
Same author

[A Case of Pathological Complete Response Post‒Pembrolizumab Therapy for Recurrent Liver Metastasis of Ascending Colon Cancer].

Gan to kagaku ryoho. Cancer & chemotherapy·2025
Same author

Expanding diverse horizons in smooth muscle research: a symposium review of "Muscle and Pathology/Health: Frontiers of Translational Research" at the 66th Annual Meeting of Japan Society of Smooth Muscle Research.

Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi·2025

Related Experiment Video

Updated: Jun 28, 2025

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles
06:58

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles

Published on: October 18, 2024

664

Abemaciclib and Vacuolin-1 decrease aggregate-prone TDP-43 accumulation by accelerating autophagic flux.

Yoshinori Tanaka1, Lina Kozuma1, Hirotsugu Hino2

  • 1Biochemistry Unit, Faculty of Veterinary Medicine, Okayama University of Science, Imabari-shi, Ehime, Japan.

Biochemistry and Biophysics Reports
|April 10, 2024
PubMed
Summary

Abemaciclib and vacuolin-1 accelerate cellular degradation of aggregate-prone TDP-43 by enhancing autophagosome formation and fusion with lysosomes, a process dependent on PI(3)P.

Keywords:
AbemaciclibAutophagic fluxPI(3)PTDP-43Vacuolin-1

More Related Videos

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

7.2K
Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain
10:08

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain

Published on: August 28, 2012

11.8K

Related Experiment Videos

Last Updated: Jun 28, 2025

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles
06:58

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles

Published on: October 18, 2024

664
siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

7.2K
Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain
10:08

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain

Published on: August 28, 2012

11.8K

Area of Science:

  • Cell Biology
  • Neuroscience
  • Molecular Biology

Background:

  • Autophagy is a key cellular process for degrading unwanted materials, including aggregate-prone TDP-43.
  • TDP-43 aggregation is implicated in neurodegenerative diseases like amyotrophic lateral sclerosis and frontotemporal lobar degeneration.
  • Abemaciclib (Abe) and vacuolin-1 (Vac) are known to induce autophagosome-lysosome structures, suggesting a role in autophagy.

Purpose of the Study:

  • To investigate if Abemaciclib and vacuolin-1 accelerate autophagic flux and reduce TDP-43 accumulation.
  • To elucidate the mechanism by which Abe and Vac influence autophagosome-lysosome fusion and TDP-43 degradation.

Main Methods:

  • Utilized SH-SY5Y neuroblastoma cells expressing autophagic flux and lysosome markers (GFP-LC3-RFP-LC3ΔG, mCherry-LC3, LAMP1-GFP).
  • Assessed autophagosome formation, lysosomal localization, and TDP-43 levels following Abe and Vac treatment.
  • Employed a PI(3)P reporter assay and a VPS34 inhibitor (wortmannin) to examine pathway involvement.

Main Results:

  • Abe and Vac dose-dependently reduced the GFP/RFP ratio, indicating accelerated autophagic flux.
  • These treatments increased autophagosome markers colocalized with lysosomes and enhanced PI(3)P signaling on lysosomes.
  • Abe and Vac treatment inhibited TDP-43 accumulation in an autophagy-dependent manner, and wortmannin blocked these effects.

Conclusions:

  • Abemaciclib and vacuolin-1 promote the degradation of aggregate-prone TDP-43.
  • These drugs enhance autophagy by increasing PI(3)P formation, thereby accelerating autophagosome formation and lysosome fusion.
  • The findings suggest a therapeutic potential for Abe and Vac in neurodegenerative diseases linked to TDP-43 aggregation.