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

Transmembrane signalling by interferon-alpha.

L M Pfeffer1, O R Colamonici

  • 1Department of Pathology, University of Tennessee Medical Center, Memphis 38163.

Pharmacology & Therapeutics
|November 1, 1991
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

MiRNA-621 sensitizes breast cancer to chemotherapy by suppressing FBXO11 and enhancing p53 activity.

Oncogene·2015
Same author

High basal NF-κB activity in nonpigmented melanoma cells is associated with an enhanced sensitivity to vitamin D3 derivatives.

British journal of cancer·2011
Same author

NF-kappaB activation mediates resistance to IFN beta in MLL-rearranged acute lymphoblastic leukemia.

Leukemia·2010
Same author

ARF-induced downregulation of Mip130/LIN-9 protein levels mediates a positive feedback that leads to increased expression of p16Ink4a and p19Arf.

Oncogene·2010
Same author

Mammalian Mip/LIN-9 interacts with either the p107, p130/E2F4 repressor complex or B-Myb in a cell cycle-phase-dependent context distinct from the Drosophila dREAM complex.

Oncogene·2007
Same author

Phosphatidylinositol 3-kinase confers resistance to encephalomyocarditis and herpes simplex virus-induced cell death through the activation of distinct downstream effectors.

Journal of immunology (Baltimore, Md. : 1950)·2001
Same journal

Nipocalimab and other FcRn blockers in neuromuscular disorders.

Pharmacology & therapeutics·2026
Same journal

C26:0-lysophosphatidylcholine in X-linked adrenoleukodystrophy.

Pharmacology & therapeutics·2026
Same journal

The CircRNA/miRNA axis in breast cancer: From molecular mechanisms to clinical translation.

Pharmacology & therapeutics·2026
Same journal

Glymphatic-meningeal lymphatic dysfunction in epilepsy: novel mechanistic insights and therapeutic avenues.

Pharmacology & therapeutics·2026
Same journal

The neurovascular unit under siege: Molecular mechanisms and potential drug target for cerebral edema.

Pharmacology & therapeutics·2026
Same journal

A-type potassium channels in pain signaling: Fundamental mechanisms and pathophysiological roles.

Pharmacology & therapeutics·2026
See all related articles

Human leukocyte interferon (IFN-alpha) alters gene expression via cell surface receptors. It activates protein kinase C (PKC) isoforms, influencing interferon-stimulated gene (ISG) transcription and antiviral defense.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Human leukocyte interferon (IFN-alpha) is a crucial cytokine that modulates cellular responses.
  • IFN-alpha exerts its effects by binding to specific cell surface receptors, initiating intracellular signaling cascades.
  • Understanding IFN-alpha's signaling pathway is vital for developing antiviral therapies and immunomodulatory strategies.

Purpose of the Study:

  • To elucidate the transmembrane signaling pathway initiated by IFN-alpha.
  • To investigate the role of protein kinase C (PKC) isoforms in IFN-alpha-mediated gene expression.
  • To determine the impact of PKC inhibition on IFN-stimulated gene (ISG) transcription and antiviral activity.

Main Methods:

  • Cell surface receptor binding assays.

Related Experiment Videos

  • Measurement of diacylglycerol (DAG) production and intracellular calcium levels.
  • Application of selective PKC inhibitors (H-7, staurosporine).
  • Analysis of IFN-stimulated gene (ISG) transcription via quantitative methods.
  • Assessment of cellular protection against viral infection.

    • Main Results:

    • IFN-alpha binding triggers DAG production without increasing intracellular calcium.
    • Calcium-independent PKC isoforms (beta and epsilon) are activated by IFN-alpha signaling.
    • Selective PKC inhibition abrogates IFN-alpha-induced ISG transcription and antiviral protection.
    • IFN-alpha induces rapid protein phosphorylation, potentially affecting latent transcription factors.

    Conclusions:

    • IFN-alpha signaling involves a DAG-dependent, calcium-independent activation of specific PKC isoforms.
    • PKC activation is essential for IFN-alpha's ability to induce ISG transcription and confer antiviral states.
    • Targeting the IFN-alpha-PKC pathway offers potential therapeutic avenues for viral infections and immune modulation.