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...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein.
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...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...

You might also read

Related Articles

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

Sort by
Same author

Disrupting Notch signalling by a small molecule inhibiting dihydroorotate dehydrogenase activity.

Scientific reports·2026
Same author

Blood safety markers in Dutch donors after relaxation of deferral for men who have sex with men: re-emergence of syphilis and HIV pre-exposure prophylaxis use.

Transfusion·2024
Same author

Retinoblastoma vulnerability to combined <i>de novo</i> and salvage pyrimidine ribonucleotide synthesis pharmacologic blockage.

Heliyon·2024
Same author

Correction: Modulation of p53 C-Terminal Acetylation by Mdm2, p14ARF, and Cytoplasmic SirT2.

Molecular cancer therapeutics·2023
Same author

Publisher Correction: A DHODH inhibitor increases p53 synthesis and enhances tumor cell killing by p53 degradation blockage.

Nature communications·2023
Same author

Correction: Proof-of-principle studies on a strategy to enhance nucleotide imbalance specifically in cancer cells.

Cell death discovery·2022
Same journal

Cancer immunotherapy with oncolytic myxoma virus.

Advances in cancer research·2026
Same journal

Cancer terminator viruses: Unique conditionally replication competent oncolytic viruses producing therapeutic anti-cancer immunomodulating agents.

Advances in cancer research·2026
Same journal

Advancing clinical translation of oncolytic adenoviruses.

Advances in cancer research·2026
Same journal

Operation oncolysis: Reoviruses in the theater of cancer war.

Advances in cancer research·2026
Same journal

AAV vectors for cancer gene therapy.

Advances in cancer research·2026
Same journal

Vesicular stomatitis virus (VSV) as an oncolytic therapeutic agent for cancer.

Advances in cancer research·2026
See all related articles

Related Experiment Video

Updated: Jun 21, 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

Sirtuins and p53.

Ingeborg van Leeuwen1, Sonia Lain

  • 1Department of Surgery and Molecular Oncology, Ninewells Hospital, University of Dundee, Dundee DD1 9SY, Scotland, United Kingdom.

Advances in Cancer Research
|July 15, 2009
PubMed
Summary
This summary is machine-generated.

Sirtuin inhibition may enhance tumor suppression by affecting p53. However, SirT1 acts as a tumor suppressor, and its inhibition can cause genomic instability, requiring safety evaluations for cancer treatments.

More Related Videos

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates
14:32

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Published on: February 27, 2016

Related Experiment Videos

Last Updated: Jun 21, 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

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates
14:32

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Published on: February 27, 2016

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Sirtuins, a class of enzymes, play a complex role in cancer, with some deacetylating tumor suppressors.
  • Human SirT1 deacetylates p53, potentially decreasing its tumor-suppressive function.
  • The precise mechanisms and implications of sirtuin-p53 interactions in cancer are under investigation.

Purpose of the Study:

  • To review and examine the regulation of p53 by sirtuins.
  • To analyze changes in sirtuin function within tumor cells.
  • To discuss the therapeutic potential and safety of sirtuin inhibition for cancer treatment.

Main Methods:

  • Literature review of existing data on sirtuin-p53 interactions.
  • Analysis of sirtuin activity in tumor cells.
  • Examination of data from SIRT1-knockout mice.

Main Results:

  • Sirtuin deacetylation of p53 may reduce its tumor-suppressive activity.
  • Sirtuin-mediated p53 regulation can occur indirectly via cellular processes.
  • SIRT1 acts as a tumor suppressor, and its sustained depletion can lead to genomic instability.

Conclusions:

  • Sirtuin inhibition might offer a strategy for cancer treatment, but its efficacy and safety require careful consideration.
  • The dual role of sirtuins, particularly SIRT1, in cancer necessitates a nuanced approach to therapeutic targeting.
  • Further research is needed to clarify the complex interplay between sirtuins, p53, and cancer development.