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

Myc protein: partners and antagonists

I Västrik1, T P Mäkelä, P J Koskinen

  • 1Department of Pathology, University of Helsinki, Finland.

Critical Reviews in Oncogenesis
|January 1, 1994
PubMed
Summary

The c-myc oncogene drives cell cycle progression and can induce apoptosis. It forms a Myc/Max heterodimer that activates genes crucial for cell growth regulation.

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

Counteracting age-related VEGF signaling insufficiency promotes healthy aging and extends life span.

Science (New York, N.Y.)·2021
Same author

Ischemia-Reperfusion Injury Enhances Lymphatic Endothelial VEGFR3 and Rejection in Cardiac Allografts.

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons·2015
Same author

Deregulated hepsin protease activity confers oncogenicity by concomitantly augmenting HGF/MET signalling and disrupting epithelial cohesion.

Oncogene·2015
Same author

Par6G suppresses cell proliferation and is targeted by loss-of-function mutations in multiple cancers.

Oncogene·2015
Same author

Donor Heart Treatment With COMP-Ang1 Limits Ischemia-Reperfusion Injury and Rejection of Cardiac Allografts.

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons·2015
Same author

Lack of cardiac and high-fat diet induced metabolic phenotypes in two independent strains of Vegf-b knockout mice.

Scientific reports·2014

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The c-myc oncogene is frequently activated in human tumors like Burkitt's lymphomas and amplified in neuroblastoma and small-cell lung cancer.
  • Myc activity is essential for normal cells to enter the cell cycle from a resting state.
  • Myc plays a dual role, driving cell cycle progression while also capable of inducing apoptosis.

Purpose of the Study:

  • To elucidate the molecular mechanisms of Myc's function in cell growth regulation.
  • To understand how Myc interacts with other proteins to regulate gene expression.

Main Methods:

  • Identification of c-myc as an oncogene in human tumors.
  • Analysis of Myc's role in cell cycle entry and apoptosis.
  • Characterization of Myc's protein domains, including its DNA-binding and dimerization capabilities.
  • Investigation of Myc's interaction with the Max protein.

Main Results:

  • Myc is a critical regulator of cell cycle entry in normal cells.
  • Myc can induce apoptosis in specific cellular contexts.
  • Myc possesses a transcriptional activation domain and a DNA-binding/dimerization domain.
  • Myc forms a sequence-specific DNA-binding heterodimer with Max.

Conclusions:

  • The Myc/Max heterodimer acts as a transcriptional activator.
  • This complex regulates genes essential for controlling cell growth.
  • Myc is a key player in both cell proliferation and programmed cell death pathways.

Related Experiment Videos