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

Proteases of the complement system.

R B Sim1, S A Tsiftsoglou

  • 1MRC Immunochemistry Unit, Department of Biochemistry, Oxford University, South Parks Road, Oxford OX1 3QU, UK. bob.sim@bioch.ox.ac.uk

Biochemical Society Transactions
|January 30, 2004
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

C2 by-pass: Cross-talk between the complement classical and alternative pathways.

Immunobiology·2022
Same author

Complement research in the 18th-21st centuries: Progress comes with new technology.

Immunobiology·2016
Same author

Complement system proteins which interact with C3b or C4b A superfamily of structurally related proteins.

Immunology today·2014
Same author

[Circulating immune complexes in families with positive history of ischemic stroke].

Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova·2008
Same author

Resistance of the Echinococcus granulosus cyst wall to complement activation: analysis of the role of InsP6 deposits.

Parasite immunology·2008
Same author

Collectins and host defence.

Novartis Foundation symposium·2007
Same journal

TDP-43 proteinopathy as a biomarker and therapeutic target in amyotrophic lateral sclerosis.

Biochemical Society transactions·2026
Same journal

Advancing the monitoring of organelle contact sites in vitro and in vivo.

Biochemical Society transactions·2026
Same journal

Mechanisms influencing transient cytoplasmic protein targeting to intracellular lipid droplets.

Biochemical Society transactions·2026
Same journal

Replication associated nuclear DNA mismatch repair across kingdoms.

Biochemical Society transactions·2026
Same journal

Phosphatases of regenerating liver downregulate PTEN to promote tumorigenesis.

Biochemical Society transactions·2026
Same journal

Implications of Rho GTPase signaling in cancer immunotherapy.

Biochemical Society transactions·2026
See all related articles

The complement system, part of innate immunity, uses proteins to eliminate microbes and damaged cells. Inhibiting its overactivation could treat inflammatory diseases.

Area of Science:

  • Immunology
  • Biochemistry

Background:

  • The complement system comprises ~35 proteins crucial for innate immunity, recognizing and eliminating pathogens and altered host cells.
  • Key recognition proteins like C1q, mannan-binding lectin (MBL), and ficolins initiate complement activation.
  • Activation cascades involve serine proteases (e.g., C1r, C1s, MASP2) leading to C3 activation, a major opsonin.

Purpose of the Study:

  • To elucidate the intricate mechanisms of complement system activation and regulation.
  • To highlight the role of complement proteases and their inhibitors in immune responses.
  • To explore the therapeutic potential of modulating complement activation in inflammatory conditions.

Main Methods:

  • Review of complement system components and their interactions.

Related Experiment Videos

  • Analysis of protease activation pathways and regulatory mechanisms.
  • Examination of complement's role in innate immunity and disease pathogenesis.
  • Main Results:

    • Complement activation involves sequential protease cascades, culminating in C3 opsonization and cell lysis.
    • Specific proteases (Factors D, I, B, C2) have unique activation and regulatory properties.
    • Excessive complement activation is linked to inflammatory diseases like rheumatoid arthritis and ischemia/reperfusion injury.

    Conclusions:

    • Understanding complement regulation is vital for controlling inflammation and associated tissue damage.
    • Targeting key protease complexes, such as C3bBb and C4b2a, offers potential therapeutic strategies.
    • Modulating complement activation presents a promising avenue for treating inflammatory and autoimmune diseases.