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

A lymphotoxin-beta-specific receptor

P D Crowe1, T L VanArsdale, B N Walter

  • 1Division of Biomedical Sciences, University of California, Riverside 92521.

Science (New York, N.Y.)
|April 29, 1994
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

Substrates enhance autophosphorylation and activation of p21-activated protein kinase gamma-PAK in the absence of activation loop phosphorylation.

European journal of biochemistry·2000
Same author

CD154 variants associated with hyper-IgM syndrome can form oligomers and trigger CD40-mediated signals.

The Journal of biological chemistry·1999
Same author

Expression of the lymphotoxin beta receptor on follicular stromal cells in human lymphoid tissues.

Cell death and differentiation·1999
Same author

Cleavage and activation of p21-activated protein kinase gamma-PAK by CPP32 (caspase 3). Effects of autophosphorylation on activity.

The Journal of biological chemistry·1998
Same author

The lymphotoxin-alpha (LTalpha) subunit is essential for the assembly, but not for the receptor specificity, of the membrane-anchored LTalpha1beta2 heterotrimeric ligand.

The Journal of biological chemistry·1997
Same author

Lymphotoxin-beta receptor signaling complex: role of tumor necrosis factor receptor-associated factor 3 recruitment in cell death and activation of nuclear factor kappaB.

Proceedings of the National Academy of Sciences of the United States of America·1997
Same journal

Erratum for the Research Article "Detecting supramolecular organic nanoparticles during heat wave".

Science (New York, N.Y.)·2026
Same journal

Local signals, systemic decline.

Science (New York, N.Y.)·2026
Same journal

The mechanics of liver regeneration.

Science (New York, N.Y.)·2026
Same journal

Computing in a memory with physics.

Science (New York, N.Y.)·2026
Same journal

Retraction.

Science (New York, N.Y.)·2026
Same journal

Making time.

Science (New York, N.Y.)·2026
See all related articles

Tumor necrosis factor (TNF) and lymphotoxin-alpha (LT-alpha) are key immune regulators. A newly identified receptor for LT-beta suggests distinct functions for cell surface LT compared to secreted LT-alpha.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Tumor necrosis factor (TNF) and lymphotoxin-alpha (LT-alpha) are crucial cytokines involved in immune and inflammatory responses.
  • LT-alpha exists in both secreted (homotrimer) and cell-surface (heteromeric complex with LT-beta) forms.
  • Secreted LT-alpha binds 60/80 kDa TNF receptors, which do not recognize the cell-surface LT-alpha-LT-beta complex.

Discussion:

  • The identification of a specific receptor for human LT-beta indicates unique signaling pathways for cell-surface LT.
  • This suggests that the functions of cell-surface LT may differ significantly from those of secreted LT-alpha.
  • Investigating the LT-beta receptor is key to understanding cell-surface LT-mediated immune regulation.

Key Insights:

  • A novel receptor specific to human lymphotoxin-beta (LT-beta) has been identified.

Related Experiment Videos

  • This discovery differentiates the signaling capabilities of cell-surface LT complexes from secreted LT-alpha.
  • The distinct receptor implies unique biological roles for cell-surface LT in immune regulation.
  • Outlook:

    • Further research into the LT-beta receptor and its downstream signaling will elucidate cell-surface LT functions.
    • Understanding these distinct pathways could reveal new therapeutic targets for immune and inflammatory diseases.
    • Comparative studies of secreted vs. cell-surface LT signaling are warranted.