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

Abnormal Proliferation02:23

Abnormal Proliferation

4.0K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.0K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

5.0K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
5.0K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

1.8K
1.8K
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

5.1K
DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
5.1K
Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

6.3K
Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
6.3K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

8.5K
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...
8.5K

You might also read

Related Articles

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

Sort by
Same author

Void-X: A generative void-filling model for predicting atomic packing in proteins.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Glucose hypometabolism and hyperphosphorylated Tau synergistically drive neuronal necroptosis.

Neuron·2026
Same author

Pharmacological strategies targeting chaperone-mediated autophagy.

Trends in pharmacological sciences·2026
Same author

Cell death in cancer.

Cell·2026
Same author

Electric dipole moment drives the dynamics of the TNFR1 complex I signalosome.

Nature·2026
Same author

CD8<sup>+</sup> T cell loss induces autoinflammation in inborn errors of cell death.

Nature communications·2026

Related Experiment Video

Updated: May 6, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

8.9K

A degradative detour for mutant TP53.

Helin Vakifahmetoglu-Norberg1, Junying Yuan

  • 1Department of Cell Biology, Harvard Medical School, Boston, MA USA.

Autophagy
|October 23, 2013
PubMed
Summary
This summary is machine-generated.

Blocking macroautophagy during nutritional stress degrades mutant TP53 via chaperone-mediated autophagy (CMA) in nonproliferating cancer cells. This suggests activating CMA as a novel cancer therapy targeting mutant TP53.

Keywords:
autophagycancerchaperone-mediated autophagymutant TP53spautin-1

More Related Videos

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

400
Gene-targeted Random Mutagenesis to Select Heterochromatin-destabilizing Proteasome Mutants in Fission Yeast
07:18

Gene-targeted Random Mutagenesis to Select Heterochromatin-destabilizing Proteasome Mutants in Fission Yeast

Published on: May 15, 2018

10.0K

Related Experiment Videos

Last Updated: May 6, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

8.9K
Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

400
Gene-targeted Random Mutagenesis to Select Heterochromatin-destabilizing Proteasome Mutants in Fission Yeast
07:18

Gene-targeted Random Mutagenesis to Select Heterochromatin-destabilizing Proteasome Mutants in Fission Yeast

Published on: May 15, 2018

10.0K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • Mutant TP53 protein accumulation drives cancer progression and metastasis.
  • Targeting mutant TP53 degradation presents a potential therapeutic strategy for cancer treatment.

Purpose of the Study:

  • To investigate the role of macroautophagy inhibition in mutant TP53 degradation.
  • To explore chaperone-mediated autophagy (CMA) as a mechanism for clearing mutant TP53.
  • To assess the therapeutic potential of activating CMA for mutant TP53-driven cancers.

Main Methods:

  • Cancer cells were subjected to nutritional stress.
  • Macroautophagy was inhibited under these conditions.
  • Chaperone-mediated autophagy (CMA) activation was monitored.
  • Mutant TP53 protein levels were assessed.

Main Results:

  • Inhibition of macroautophagy under nutritional stress induced mutant TP53 degradation.
  • This degradation was mediated by the activation of the chaperone-mediated autophagy (CMA) pathway.
  • The effect was observed in nonproliferating cancer cells.

Conclusions:

  • Chaperone-mediated autophagy (CMA) represents a novel pathway for mutant TP53 degradation.
  • Activating CMA could be a new therapeutic approach for cancers harboring mutant TP53.
  • Targeting CMA offers a promising strategy for improving outcomes in specific cancer types.