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

The CD95 type I/type II model.

Bryan C Barnhart1, Elizabeth C Alappat, Marcus E Peter

  • 1The Ben May Institutefor Cancer Research, University of Chicago, 924 E. 57th Street, Chicago, IL 60637, USA.

Seminars in Immunology
|October 18, 2003
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

Developing a pan cancer therapy based on DISE-inducing short RNAs.

Molecular therapy. Nucleic acids·2026
Same author

Unfolding a death signal to treat rheumatoid arthritis.

Nature materials·2024
Same author

Corrigendum: miR-182 integrates apoptosis, growth, and differentiation programs in glioblastoma.

Genes & development·2024
Same author

Death Induced by Survival gene Elimination (DISE) correlates with neurotoxicity in Alzheimer's disease and aging.

Nature communications·2024
Same author

DISE, an ancient anti-cancer mechanism that senses mutational load in cancerous cells?

Oncotarget·2023
Same author

Cancer kill code extension.

Molecular therapy. Nucleic acids·2023
Same journal

Myeloid cells as sources and targets of IL-1 family cytokines in cancer.

Seminars in immunology·2026
Same journal

Interleukin-1-mediated inflammatory memory: Protective training or maladaptive tumor imprinting?

Seminars in immunology·2026
Same journal

Chronic stress at the crossroads: Decoding the HPA-SAM-immune-gut axis in inflammatory bowel disease pathogenesis and therapeutics.

Seminars in immunology·2026
Same journal

Protein tyrosine kinases in dendritic cell-mediated anti-cancer immunity.

Seminars in immunology·2026
Same journal

The immune system in Latin America and the Caribbean: Insights into diseases and diversity from local perspectives.

Seminars in immunology·2026
Same journal

Introduction to the special issue: T<sub>H</sub>9 cells in diseases.

Seminars in immunology·2026
See all related articles

CD95 (APO-1/Fas) receptor initiates apoptosis via extrinsic and intrinsic pathways. This review details the cross-talk between these CD95-mediated cell death routes, distinguishing Type I and Type II cells.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • CD95 (APO-1/Fas) is a key death receptor initiating the extrinsic apoptosis pathway.
  • The extrinsic pathway involves caspase-8 activation within the death-inducing signaling complex (DISC).
  • The intrinsic pathway originates intracellularly, involving mitochondrial factors and caspase-9 activation in the apoptosome.

Purpose of the Study:

  • To review recent advancements in understanding CD95-mediated apoptosis.
  • To delineate the biochemistry and physiological functions of CD95's extrinsic and intrinsic pathways.
  • To explore the cross-talk mechanisms between the extrinsic and intrinsic apoptosis pathways.

Main Methods:

  • Literature review of recent developments in apoptosis research.

Related Experiment Videos

  • Analysis of biochemical mechanisms governing CD95 signaling.
  • Comparison of Type I and Type II cell death responses mediated by CD95.
  • Main Results:

    • Identified CD95 as a prototype death receptor activating the extrinsic apoptosis pathway.
    • Described the intrinsic apoptosis pathway initiated by intracellular events and mitochondrial factors.
    • Highlighted the cross-talk between extrinsic and intrinsic pathways, notably via Bid cleavage by caspase-8.

    Conclusions:

    • CD95 signaling involves complex interactions between extrinsic and intrinsic apoptosis pathways.
    • Bid acts as a crucial link, connecting caspase-8 activity to mitochondrial events.
    • Cells are classified as Type I or Type II based on their reliance on mitochondrial support for CD95-induced death.