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Related Concept Videos

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...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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...
Positive Regulator Molecules02:39

Positive Regulator Molecules

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.
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
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.

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Cell Cycle-specific Measurement of &#947;H2AX and Apoptosis After Genotoxic Stress by Flow Cytometry
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Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry

Published on: September 1, 2019

Alternative cyclin D1 splice forms differentially regulate the DNA damage response.

Zhiping Li1, Xuanmao Jiao, Chenguang Wang

  • 1Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.

Cancer Research
|October 14, 2010
PubMed
Summary

Cyclin D1a protein enhances the DNA damage response (DDR) by promoting DNA repair and cell cycle arrest. Its absence or reduction impairs the DDR, highlighting its crucial role in cancer progression and treatment.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Cycle Regulation

Background:

  • The DNA damage response (DDR) is critical for maintaining genomic stability and involves cell cycle checkpoints.
  • Cyclin D1 overexpression is common in human cancers and plays a role in tumor development.
  • Alternative splicing of the cyclin D1 gene produces D1a and D1b protein isoforms with distinct functions.

Purpose of the Study:

  • To investigate the role of cyclin D1, specifically the D1a splice variant, in regulating the DNA damage response (DDR).
  • To elucidate the mechanisms by which cyclin D1a influences DDR activation and DNA repair processes.

Main Methods:

  • Overexpression of cyclin D1a in cells to assess its impact on DDR markers like γH2AX phosphorylation and DNA repair foci.
  • Gene deletion or small interfering RNA (siRNA) to reduce endogenous cyclin D1 levels in cancer cells.
  • Chromatin association studies to determine the localization and function of cyclin D1a during DDR.

Main Results:

  • Cyclin D1a overexpression enhanced the DDR, evidenced by increased γH2AX phosphorylation, DNA repair foci assembly, and G(2)-M cell cycle arrest.
  • Reduction of cyclin D1 levels impaired the DDR and compromised the cellular response to DNA-damaging agents like 5-fluorouracil.
  • Mechanistic data revealed that cyclin D1a, similar to DNA repair factors, elicits the DDR upon stable chromatin association.

Conclusions:

  • Cyclin D1a is a key regulator of the DNA damage response, promoting DNA repair and cell cycle arrest.
  • The findings suggest that cyclin D1a plays a significant role in cancer cell survival and response to genotoxic stress.
  • Targeting cyclin D1a could represent a therapeutic strategy for enhancing cancer treatment efficacy.