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

ICE-like proteases execute the neuronal death program

J C Martinou1, R Sadoul

  • 1Geneva Biomedical Research Institute, Glaxo Wellcome Research and Development S.A, Switzerland. jcm26619@ggr.co.uk

Current Opinion in Neurobiology
|October 1, 1996
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

Constitutive p53 heightens mitochondrial apoptotic priming and favors cell death induction by BH3 mimetic inhibitors of BCL-xL.

Cell death & disease·2017
Same author

Constitutive p53 heightens mitochondrial apoptotic priming and favors cell death induction by BH3 mimetic inhibitors of BCL-xL.

Cell death & disease·2016
Same author

Mitochondria and cancer: is there a morphological connection?

Oncogene·2006
Same author

Exosomes are released by cultured cortical neurones.

Molecular and cellular neurosciences·2006
Same author

Early increase of apoptosis-linked gene-2 interacting protein X in areas of kainate-induced neurodegeneration.

Neuroscience·2004
Same author

The p75 neurotrophin receptor: effects on neuron survival in vitro and interaction with death domain-containing adaptor proteins.

Apoptosis : an international journal on programmed cell death·2003

Scientists have identified key proteases, like ced-3 and interleukin-1 beta-converting enzyme, that cause neuron death during programmed cell death. These findings offer new therapeutic targets for nervous system disorders.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Programmed cell death, or apoptosis, is crucial for development and tissue homeostasis.
  • Dysregulation of neuronal apoptosis is implicated in various neurological diseases.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying neuronal death in programmed cell death.
  • To identify key molecular players involved in executing neuronal apoptosis.

Main Methods:

  • Utilized genetic studies in *Caenorhabditis elegans* to identify essential genes for programmed cell death.
  • Investigated the role of specific proteases, including ced-3 and mammalian interleukin-1 beta-converting enzyme, in neuronal apoptosis.

Main Results:

Related Experiment Videos

  • Identified a family of proteases, initiated by ced-3, as critical executioners of programmed cell death.
  • Demonstrated that these proteases are conserved across species, from nematodes to mammals.

    • Conclusions:

    • The identified proteases represent a conserved mechanism for neuronal apoptosis.
    • These proteases are promising therapeutic targets for treating neurological conditions characterized by neuronal loss.