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

Identification of defensin binding to C1 complement

A V Panyutich1, O Szold, P H Poon

  • 1Will Rogers Pulmonary Research Laboratory, University of California at Los Angeles 90024-1736.

FEBS Letters
|December 19, 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

Coexistence of Insulatorlike Paramagnon and Metallic Spin-Orbit Exciton Modes in SrIrO_{3}.

Physical review letters·2025
Same author

Magnon interactions in a moderately correlated Mott insulator.

Nature communications·2024
Same author

Fate of charge order in overdoped La-based cuprates.

npj quantum materials·2024
Same author

Hepcidin-The Culprit Explaining Disturbed Iron Homeostasis in Chronic Renal Disease?: IL-6 Mediates Hypoferremia of Inflammation by Inducing the Synthesis of the Iron Regulatory Hormone Hepcidin. J Clin Invest 113:1271-1276, 2004.

Journal of the American Society of Nephrology : JASN·2023
Same author

Publisher Correction: Electronic structure of the parent compound of superconducting infinite-layer nickelates.

Nature materials·2020
Same author

High-Temperature Charge-Stripe Correlations in La_{1.675}Eu_{0.2}Sr_{0.125}CuO_{4}.

Physical review letters·2020
Same journal

Regulation of CFTR stability at the plasma membrane-Mechanisms and therapeutic opportunities in cystic fibrosis.

FEBS letters·2026
Same journal

Identification of a Shiga toxin A-derived peptide internalized into Gb3 receptor-bearing cells via interaction with the Shiga toxin B subunit.

FEBS letters·2026
Same journal

The dual role of lectins in cancer-immunotherapy tools and therapeutic targets.

FEBS letters·2026
Same journal

Decoding the dynamic extracellular matrix in cancer-3D models and bioscaffolds rewire the rules of tumor progression.

FEBS letters·2026
Same journal

Extending the classical sequence-structure-function paradigm through protein dynamics and context-dependent behavior.

FEBS letters·2026
Same journal

α-Synuclein aggregation landscape from phase separation to neurotoxic intermediates.

FEBS letters·2026
See all related articles

Defensins bind to activated complement C1 complexes in human serum, bridging innate immunity pathways. This interaction may protect tissues from defensin-induced injury during infection.

Area of Science:

  • Immunology
  • Biochemistry

Background:

  • Defensins are antimicrobial peptides crucial for host defense.
  • The complement system is a key component of innate immunity.
  • Interactions between complement and antimicrobial peptides are not fully understood.

Purpose of the Study:

  • To investigate the binding of defensins to components of the C1 complement complex.
  • To elucidate the role of C1 complexes in bridging complement and phagocyte-mediated defenses.

Main Methods:

  • Analysis of human serum for defensin binding to activated C1 complement (C1) and C1 inhibitor (C1i).
  • Testing of purified C1q, activated C1 tetramer (r2s2), and C1i for defensin binding.
  • Dissociation of r2s2 using EDTA to identify specific binding partners.

Related Experiment Videos

Main Results:

  • Strong defensin binding was observed with complexes of activated C1 and C1 inhibitor in human serum.
  • Purified C1q, r2s2, and C1i did not bind defensin.
  • Upon dissociation of r2s2, only activated C1s demonstrated defensin binding.

Conclusions:

  • Defensin binding to activated C1 complement represents a novel link between complement and phagocyte-mediated immunity.
  • This interaction may serve as a protective mechanism against cytotoxic injury by defensins in infected tissues.