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

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 daughter...
Metabolic States of the Body: Fasting and Starvation01:24

Metabolic States of the Body: Fasting and Starvation

During the initial hours of fasting, the body uses up its glycogen stores as an energy source. Once these glycogen reserves are depleted, the body begins breaking down stored triglycerides and structural proteins. During this stage, glycerol becomes a key substrate for gluconeogenesis, while free fatty acids undergo beta-oxidation to provide energy for tissues, such as skeletal muscle. In the fasting state, the body spares protein breakdown as much as possible to conserve muscle and structural...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
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...
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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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...

You might also read

Related Articles

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

Sort by
Same author

Cell-free therapy for alopecia via the secretome of hiPSC-derived dermal papilla cells.

Journal of tissue engineering·2026
Same author

Multimodal AI mapping with GigaTIME reveals spatial immune signaling states in the tumor microenvironment.

International journal of biological sciences·2026
Same author

Toward animal-free cardiac safety testing: Early detection of cardiotoxic reactions via multimodal in vitro readouts.

Journal of advanced research·2026
Same author

CD47-mediated purification of human ventricular cardiomyocytes derived from pluripotent stem cells.

Animal cells and systems·2026
Same author

Cultivated Meat and the Future of Food Systems: Promise, Progress, and Challenges.

Food science & nutrition·2026
Same author

Toxicological perspectives on potential mixture toxicity of alpha-hexylcinnamaldehyde and lilial in consumer products.

Toxicology mechanisms and methods·2026
Same journal

Circular RNA circ_0001829 attenuates G2/M arrest to promote hepatocyte proliferation by sponging miR-3095-3p following liver injury.

Cell cycle (Georgetown, Tex.)·2026
Same journal

Identification of PGF+ endothelial cells associated with plaque instability in carotid atherosclerosis by scRNA-seq and RNA-seq analysis.

Cell cycle (Georgetown, Tex.)·2026
Same journal

BMSCs-derived exosomal miR-196a-5p promotes macrophage M2 polarization and osteogenesis in postmenopausal osteoporosis through regulating Rspo2/Wnt/β-catenin signaling.

Cell cycle (Georgetown, Tex.)·2026
Same journal

MicroRNA-6833-3p drives prostate cancer progression and stemness by targeting the NUMB-mediated NOTCH signaling pathway.

Cell cycle (Georgetown, Tex.)·2026
Same journal

OTUD5 promotes AML progression by stabilizing SLC7A11 to suppress ferroptosis.

Cell cycle (Georgetown, Tex.)·2026
Same journal

MITF-Driven melanoma plasticity as a core mechanism of therapy resistance: integrating microenvironmental signaling, mechanotransduction, and metabolic reprogramming.

Cell cycle (Georgetown, Tex.)·2026
See all related articles

Related Experiment Video

Updated: May 14, 2026

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

Mutant p53 succumbs to starvation

Sung-Hwan Moon1, Carol Prives

  • 1Department of Biological Sciences, Columbia University, New York, NY, USA.

Cell Cycle (Georgetown, Tex.)
|February 21, 2013
PubMed
Summary

No abstract available in PubMed .

Keywords:
acetylationautophagyglucose restrictionmutant p53proteasome

More Related Videos

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

Analyzing Starvation-Induced Autophagy in the Drosophila melanogaster Larval Fat Body
06:02

Analyzing Starvation-Induced Autophagy in the Drosophila melanogaster Larval Fat Body

Published on: August 4, 2022

Related Experiment Videos

Last Updated: May 14, 2026

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

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

Analyzing Starvation-Induced Autophagy in the Drosophila melanogaster Larval Fat Body
06:02

Analyzing Starvation-Induced Autophagy in the Drosophila melanogaster Larval Fat Body

Published on: August 4, 2022