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

5.5K
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...
5.5K
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

6.2K
Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
6.2K
Positive Regulator Molecules01:45

Positive Regulator Molecules

133.5K
To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
133.5K
Positive Regulator Molecules02:39

Positive Regulator Molecules

6.4K
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.
6.4K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

9.9K
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...
9.9K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

3.0K
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...
3.0K

You might also read

Related Articles

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

Sort by
Same author

αKG-mediated carnitine synthesis drives DNA repair via histone acetylation.

Nature·2026
Same author

RHOV Is a Detachment-Responsive Rho GTPase Necessary for Ovarian Cancer Peritoneal Metastasis.

Cancer research·2026
Same author

Uracil-DNA glycosylase deficiency is associated with repressed tumor cell-intrinsic inflammatory signaling and altered sensitivity to exogenous interferons.

NAR cancer·2026
Same author

The chemotherapy-induced senescence-associated secretome promotes cell detachment and metastatic dissemination through metabolic reprogramming.

bioRxiv : the preprint server for biology·2025
Same author

RHOV is a Detachment-Responsive Rho GTPase Necessary for Ovarian Cancer Peritoneal Metastasis.

bioRxiv : the preprint server for biology·2025
Same author

Loss of Predicted Cell Adhesion Molecule MPZL3 Promotes EMT in Ovarian Cancer.

Cancer research communications·2025

Related Experiment Video

Updated: Jan 4, 2026

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes
05:22

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes

Published on: April 13, 2018

10.9K

p16: cycling off the beaten path.

Raquel Buj1, Katherine M Aird1

  • 1Department of Cellular & Molecular Physiology, Penn State College of Medicine, Hershey, PA, USA.

Molecular & Cellular Oncology
|November 7, 2019
PubMed
Summary
This summary is machine-generated.

p16INK4A (p16) is a key tumor suppressor. Beyond its known role, p16 also influences nucleotide metabolism, revealing new anti-cancer functions.

Keywords:
AP-1JNK1/3NF-κBRetinoblastomaSP1cell cyclemTORC1nucleotide metabolismreactive oxygen speciessenescence

More Related Videos

Analysis of Cell Cycle Position in Mammalian Cells
12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

61.2K
Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

28.2K

Related Experiment Videos

Last Updated: Jan 4, 2026

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes
05:22

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes

Published on: April 13, 2018

10.9K
Analysis of Cell Cycle Position in Mammalian Cells
12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

61.2K
Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

28.2K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • p16INK4A (p16) is a well-established tumor suppressor.
  • Its canonical function involves the retinoblastoma (RB) pathway.
  • Emerging evidence suggests RB-independent roles for p16.

Purpose of the Study:

  • To summarize the non-canonical functions of p16.
  • To highlight recent findings on p16's role in nucleotide metabolism.

Main Methods:

  • Literature review of p16 functions.
  • Experimental investigation of p16 in nucleotide metabolism (details not provided in abstract).

Main Results:

  • p16 exhibits functions beyond the canonical RB pathway.
  • p16 plays a role in nucleotide metabolism.

Conclusions:

  • p16 has diverse, non-canonical roles in cellular processes.
  • Understanding these novel functions may reveal new therapeutic strategies against cancer.