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

Regulators of cell death

S J Korsmeyer1

  • 1Department of Medicine and Pathology, Howard Hughes Medical Institute, Washington University School of Medicine, Saint Louis, MO 63110, USA.

Trends in Genetics : TIG
|March 1, 1995
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

Tuberin activates the proapoptotic molecule BAD.

Oncogene·2006
Same author

BH3 peptidomimetics potently activate apoptosis and demonstrate single agent efficacy in neuroblastoma.

Oncogene·2006
Same author

Bax regulates c-Myc-induced mammary tumour apoptosis but not proliferation in MMTV-c-myc transgenic mice.

British journal of cancer·2004
Same author

Expression of apoptosis inhibitor protein Mcl1 linked to neuroprotection in CNS neurons.

Cell death and differentiation·2004
Same author

BCLW mediates survival of postmitotic Sertoli cells by regulating BAX activity.

Developmental biology·2002
Same author

BAX contributes to apoptotic-like death following neonatal hypoxia-ischemia: evidence for distinct apoptosis pathways.

Molecular medicine (Cambridge, Mass.)·2002
Same journal

The future of marsupial gene editing: What's in the (tool) pouch?

Trends in genetics : TIG·2026
Same journal

Genetic suppressors as new therapeutic targets for Mendelian diseases.

Trends in genetics : TIG·2026
Same journal

Beyond housekeeping: snRNA diversity, regulation, and human disease.

Trends in genetics : TIG·2026
Same journal

Rethinking mitochondrial metabolism: Intraindividual variability meets population constraints.

Trends in genetics : TIG·2026
Same journal

A role for epigenetics in rapid adaptation.

Trends in genetics : TIG·2026
Same journal

The myth of asexual fungi.

Trends in genetics : TIG·2026
See all related articles

The Bcl-2 protein represses cell death, while Bax promotes it. Their balance is crucial for preventing excessive cell death in multicellular organisms.

Area of Science:

  • Molecular biology
  • Cellular biology
  • Developmental biology

Background:

  • The Bcl-2 protein is a novel oncogene-derived protein.
  • Bcl-2 acts as a repressor of cell death.
  • Cellular suicide pathways are conserved across multicellular animals.

Purpose of the Study:

  • To investigate the role of Bcl-2 in regulating cell death.
  • To understand the interaction between Bcl-2 and Bax.
  • To determine the consequences of Bcl-2 deficiency in vivo.

Main Methods:

  • Utilizing Bcl-2-deficient mice models.
  • Analyzing the molecular interactions between Bcl-2 and Bax through conserved motifs (BH1 and BH2).
  • Observing cellular phenotypes in different cell types.

Related Experiment Videos

Main Results:

  • Bcl-2 acts as a critical repressor in the cell death pathway.
  • Bax, a related protein, promotes cell death and interacts with Bcl-2.
  • Bcl-2 deficiency leads to a reset molecular ratio, causing massive cell death in multiple cell types.

Conclusions:

  • The balance between Bcl-2 and Bax is essential for regulating cell death.
  • Dysregulation of this balance can lead to widespread cellular apoptosis.
  • Bcl-2 plays a fundamental role in preventing excessive cell death in multicellular organisms.