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

5.4K
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...
5.4K
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

6.1K
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...
6.1K
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
Positive Regulator Molecules01:45

Positive Regulator Molecules

128.6K
To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
128.6K
Abnormal Proliferation02:23

Abnormal Proliferation

5.0K
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...
5.0K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.8K
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...
9.8K

You might also read

Related Articles

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

Sort by
Same author

Performance evaluation of SFP models using ML/DL and feature selection via cost evaluation framework.

Scientific reports·2026
Same author

The landscape of plasma proteomic links to human organ imaging.

Nature communications·2026
Same author

Factors Associated With Retinal Nerve Fiber Layer Asymmetry in Primary Open-Angle Glaucoma Among Individuals of African Ancestry.

Journal of glaucoma·2026
Same author

Investigating therapeutic response to netarsudil in glaucoma subjects with the <i>ARHGEF12</i> risk variant.

Frontiers in pharmacology·2026
Same author

Variant-to-gene mapping identifies <i>ARHGEF12</i> as a primary open-angle glaucoma effector gene operating within retinal ganglion cells.

bioRxiv : the preprint server for biology·2026
Same author

Identification of novel blood-borne soluble binding partners of factor H-related proteins.

Scientific reports·2026

Related Experiment Video

Updated: Dec 11, 2025

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
09:08

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer

Published on: January 12, 2020

7.1K

Molecular Genetics and Functional Analysis Implicate CDKN2BAS1-CDKN2B Involvement in POAG Pathogenesis.

Sonika Rathi1, Ian Danford1,2, Harini V Gudiseva1

  • 1Scheie Eye Institute, Department of Ophthalmology, Philadelphia, PA 19104, USA.

Cells
|August 23, 2020
PubMed
Summary

The CDKN2B-AS1 gene is linked to primary open-angle glaucoma (POAG). Suppressing CDKN2B-AS1 increases CDKN2B, potentially causing trabecular meshwork cell senescence and POAG.

Keywords:
African AmericansCDKN2B-AS1Primary open-angle glaucoma (POAG)senescencetrabecular meshwork cells

More Related Videos

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
12:26

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

19.2K
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

7.9K

Related Experiment Videos

Last Updated: Dec 11, 2025

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
09:08

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer

Published on: January 12, 2020

7.1K
Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
12:26

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

19.2K
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

7.9K

Area of Science:

  • Ophthalmology
  • Genetics
  • Molecular Biology

Background:

  • The 9p21 locus, including CDKN2B-AS1 and CDKN2B genes, is associated with Primary Open-Angle Glaucoma (POAG).
  • The functional role of this genetic locus in POAG pathogenesis remains largely unelucidated.

Purpose of the Study:

  • To investigate the functional role of the CDKN2BAS1-CDKN2B axis in the pathogenesis of POAG.
  • To explore the regulatory relationship between CDKN2B-AS1 and CDKN2B in the context of POAG.

Main Methods:

  • Genotyping of African American POAG cases and controls for CDKN2B-AS1 single nucleotide polymorphism (SNP) rs4977756.
  • Luciferase reporter assays in HEK293T cells to assess transcriptional activity.
  • siRNA-mediated knockdown of CDKN2B-AS1 in HEK293T and trabecular meshwork (TM) cells.
  • Quantitative real-time PCR (qRT-PCR) for gene expression analysis in TM cells and human POAG ocular tissues.

Main Results:

  • Significant association of CDKN2B-AS1 SNP rs4977756 with POAG and its endophenotypes (vertical cup-disc ratio, central corneal thickness).
  • The rs4977756 region functions as a transcriptional repressor.
  • Knockdown of CDKN2B-AS1 increased CDKN2B expression in cell lines and human POAG ocular tissues.
  • CDKN2B-AS1 suppression led to increased cellular senescence, TGFβ signaling, and extracellular matrix (ECM) deposition in TM cells.

Conclusions:

  • CDKN2B-AS1 acts as a regulator, potentially by modulating CDKN2B expression.
  • Elevated CDKN2B levels resulting from CDKN2B-AS1 suppression may induce trabecular meshwork cell senescence, contributing to POAG pathogenesis.