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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

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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...
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Abnormal Proliferation02:23

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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...
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Negative Regulator Molecules01:23

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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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Nucleotide Excision Repair01:38

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DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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Related Experiment Video

Updated: Nov 20, 2025

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
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MBNL2 Regulates DNA Damage Response via Stabilizing p21.

Jin Cai1,2, Ningchao Wang1,2, Guanglan Lin1,2

  • 1State Key Laboratory of Chemical Oncogenomics, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, China.

International Journal of Molecular Sciences
|January 20, 2021
PubMed
Summary

Muscleblind-like splicing regulator 2 (MBNL2) impacts cancer cell proliferation and DNA damage response. MBNL2 depletion impairs DNA repair and senescence, promoting apoptosis, via p21 regulation.

Keywords:
Chk1DNA damage responseMBNL2RNA-binding proteincancerp21

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • RNA-binding proteins regulate gene expression and are often dysregulated in cancer.
  • Aberrant DNA damage response (DDR) contributes to cancer development and progression.

Purpose of the Study:

  • To investigate the role of muscleblind-like splicing regulator 2 (MBNL2) in tumor cell proliferation and DNA damage response.
  • To elucidate the molecular mechanisms by which MBNL2 influences cancer cell fate.

Main Methods:

  • Transcriptome and gene expression analysis in MBNL2-depleted cells.
  • Western blotting to assess protein levels and phosphorylation.
  • Functional assays evaluating DNA damage repair, senescence, and apoptosis.

Main Results:

  • MBNL2 depletion enriched the PI3K/AKT pathway and affected cyclin-dependent kinase inhibitor 1A (p21) expression.
  • MBNL2 regulates p21 mRNA and protein levels independently of p53.
  • MBNL2 depletion enhanced DNA damage response, indicated by increased checkpoint kinase 1 (Chk1) phosphorylation, in a p21-dependent manner.

Conclusions:

  • MBNL2 plays a critical role in modulating tumor cell proliferation and DNA damage response.
  • MBNL2 influences cancer cell fate post-DNA damage by regulating p21, affecting DNA repair, senescence, and apoptosis.