Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Negative Regulator Molecules

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.

Abnormal Proliferation

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...

DNA Damage can Stall the Cell Cycle

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 Cycle

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 Activity

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...

Master Transcription Regulators

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...

You might also read

Related Articles

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

Sort by

Same author

Higher-Order Clustering of Receptors Real-Time Projected by Plasmon-ruler on the Single Live Cell.

Nano letters·2026

Same author

Plant-Plant Communication for Systemic Acquired Resistance under Biotic Stress Spatiotemporally Tracked by an <i>In Situ</i> Surface-Enhanced Raman Spectroscopy Aerosol Spraying Analyzer.

ACS sensors·2026

Same author

Associations of Dietary Patterns and Micronutrients With Major Adverse Cardiovascular Events and Mortality Among Populations With Cardiovascular-Kidney-Metabolic Syndrome Stages 0-3: Results From Two Prospective Cohorts.

Food science & nutrition·2026

Same author

Dissecting Allele-Specific Expression (ASE) in Landrace × Meishan Cross Pig Fetal-Placental Tissues: Distribution, Functional Split, and Mechanisms.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology·2026

Same author

Symmetrical Tetravalent Aptamer-Protein Conjugate with Ultrahigh <i>In Vivo</i> Stability for Targeted Cancer Imaging and Therapy.

Nano letters·2026

Same author

Transcription factor, E4BP4, inhibits autophagy and apoptosis in multiple myeloma and promotes the HDAC3-mediated suppression of the Beclin1 promoter to reduce dexamethasone sensitivity.

Journal of translational medicine·2026

Search research articles

Related Experiment Video

Updated: Jun 27, 2026

Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry

Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry

Published on: May 17, 2016

Zfp36l1 Inhibits DNA Damage by Regulating p21-E2F1-Rad51 Signaling During Myogenic Differentiation.

Yi Liu¹, Xiaoyu Jiang², Jingxin Sun¹

¹Key Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.

International Journal of Molecular Sciences

|June 26, 2026

Summary

The RNA-binding protein Zfp36l1 safeguards genome stability during skeletal muscle differentiation by regulating DNA damage. It ensures proper muscle development by balancing DNA breaks through the p21-E2F1-Rad51 pathway.

Keywords:

DNA damage Zfp36l1 homologous recombination myogenic differentiation p21

More Related Videos

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Published on: September 28, 2012

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

Related Experiment Videos

Last Updated: Jun 27, 2026

Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry

Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry

Published on: May 17, 2016

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Published on: September 28, 2012

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

Area of Science:

Molecular Biology
Genetics
Cell Biology

Background:

Skeletal muscle differentiation involves DNA strand breaks (DSBs), but excessive damage hinders this process.
The RNA-binding protein Zfp36l1 is involved in muscle regeneration, but its role in genome stability during differentiation is unknown.

Purpose of the Study:

To investigate the role and mechanism of Zfp36l1 in regulating DNA damage during myogenic differentiation.
To determine how Zfp36l1 influences genome stability and cell cycle progression in C2C12 myoblasts.

Main Methods:

Utilized C2C12 myoblast cells for loss- and gain-of-function assays.
Performed RNA sequencing (RNA-seq) to analyze gene expression changes.
Conducted rescue experiments to validate findings.

Main Results:

Zfp36l1 expression increases during early differentiation, coinciding with physiological DSBs.
Zfp36l1 deficiency exacerbates DSBs, cell cycle arrest, and apoptosis; overexpression attenuates these effects.
Zfp36l1 knockdown impairs homologous recombination (HR) repair by downregulating Rad51 and Brca1, and suppresses p21 expression, thereby promoting Rad51 transcription via E2F1.

Conclusions:

Zfp36l1 is crucial for maintaining genome stability during myogenic differentiation.
Zfp36l1 balances DNA damage via the p21-E2F1-Rad51 signaling axis, impacting muscle development and genomic instability-related muscle diseases.