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 Experiment Videos

How to MEK muscle.

B H Penn1, C A Berkes, D A Bergstrom

  • 1Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.

Molecular Cell
|September 8, 2001
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Evaluation of blood gene expression levels in facioscapulohumeral muscular dystrophy patients.

Scientific reports·2020
Same author

An accessible pharmacodynamic transcriptional biomarker for notch target engagement.

Clinical pharmacology and therapeutics·2016
Same author

p53 suppresses muscle differentiation at the myogenin step in response to genotoxic stress.

Cell death and differentiation·2014
Same author

Elimination of contaminating cap genes in AAV vector virions reduces immune responses and improves transgene expression in a canine gene therapy model.

Gene therapy·2014
Same author

Clinical trial preparedness in facioscapulohumeral dystrophy: outcome measures and patient access: 8-9 April 2013, Leiden, The Netherlands.

Neuromuscular disorders : NMD·2013
Same author

Phase relationships support a role for coordinated activity in the indirect pathway in organizing slow oscillations in basal ganglia output after loss of dopamine.

Neuroscience·2006
Same journal

Thyroid cancer-associated EZH1 Q571R mutation drives chromatin compaction and H3K27me3 invasion into active chromatin.

Molecular cell·2026
Same journal

Genome-wide rotational and translational phasing of nucleosomes with human transcription factors.

Molecular cell·2026
Same journal

Spliceosomal proofreading factors safeguard 3' splice-site fidelity and prevent proteotoxicity and inflammation.

Molecular cell·2026
Same journal

Cytosolic EZH2-IMPDH2 complexes regulate melanoma progression and metastasis via GTP.

Molecular cell·2026
Same journal

A bacterial reverse transcriptase: Protein-templated DNA synthesis fuels antiviral immunity.

Molecular cell·2026
Same journal

Tweezing apart ribosome heterogeneity.

Molecular cell·2026
See all related articles

Receptor activation of Ras inhibits muscle development by affecting MEK and ERK kinases. Perry et al. reveal that activated MEK1 forms an inhibitory complex with nuclear myogenic transcription factors, clarifying this mechanism.

Area of Science:

  • Molecular biology
  • Cell signaling
  • Muscle development

Background:

  • Receptor activation of Ras signaling pathway is known to inhibit myogenesis.
  • The precise molecular mechanisms by which Ras-activated MEK and ERK kinases impede muscle differentiation remain incompletely understood.

Purpose of the Study:

  • To elucidate the mechanism by which Ras-activated MEK and ERK kinases inhibit myogenesis.
  • To identify the specific molecular interactions involved in the inhibition of myogenic transcription factors.

Main Methods:

  • Cellular and molecular biology techniques
  • Biochemical assays
  • Confocal microscopy

Main Results:

  • Activated MEK1 kinase forms a stable inhibitory complex with key myogenic transcription factors, including MyoD and Myogenin.

Related Experiment Videos

  • This complex formation sequesters myogenic transcription factors in the nucleus, preventing their transcriptional activity.
  • The inhibitory complex formation is dependent on the kinase activity of MEK1.
  • Conclusions:

    • Activated MEK1 directly inhibits myogenesis by forming an inhibitory complex with myogenic transcription factors in the nucleus.
    • This finding provides a novel mechanistic link between Ras/MEK/ERK signaling and muscle differentiation.
    • Targeting the MEK1-myogenic transcription factor interaction could offer therapeutic strategies for muscle-related disorders.