Jove
Visualize
Contact Us

Related Concept Videos

Complement System01:27

Complement System

2.0K
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
2.0K
IP3/DAG Signaling Pathway01:11

IP3/DAG Signaling Pathway

11.7K
Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
11.7K
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

8.2K
When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
8.2K
Amplifying Signals via Second Messengers01:15

Amplifying Signals via Second Messengers

6.6K
Many receptor binding ligands are hydrophilic; they do not cross the cell membrane but bind to cell-surface receptors. Thus, their message must be relayed by second messengers present in the cell cytoplasm. There are several second messenger pathways, each with its own way of relaying information. For example, the G protein-coupled receptors can activate both phosphoinositol and cyclic AMP (cAMP) second messenger pathways. The phosphoinositol pathway is active when the receptor induces...
6.6K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

5.7K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
5.7K
Antigen Processing Pathways01:31

Antigen Processing Pathways

862
MHC molecules are key players in the immune response, enabling T cells to recognize and respond to specific antigens. They are present on the surface of all nucleated cells in the body and are instrumental in presenting antigens to T cells and activating them. T cells recognize the MHC-antigen complex and initiate an immune response. MHC class I and MHC class II are two main types of MHC molecules, each associated with a distinct antigen processing pathway.
MHC Class I: Presenting Endogenous...
862

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Structural basis for independent pore function of Vpb4 from Bacillus thuringiensis.

Nature communications·2026
Same author

Inhibiting heme piracy by pathogenic Escherichia coli using de novo-designed proteins.

Nature communications·2025
Same author

The neoepitope of the complement C5b-9 Membrane Attack Complex is formed by proximity of adjacent ancillary regions of C9.

Communications biology·2023
Same author

Cryo-electron tomography: an ideal method to study membrane-associated proteins.

Philosophical transactions of the Royal Society of London. Series B, Biological sciences·2017
Same author

The mystery behind membrane insertion: a review of the complement membrane attack complex.

Philosophical transactions of the Royal Society of London. Series B, Biological sciences·2017
Same author

Stonefish toxin defines an ancient branch of the perforin-like superfamily.

Proceedings of the National Academy of Sciences of the United States of America·2015
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 Video

Updated: May 20, 2025

Functional Complementation Analysis FCA: A Laboratory Exercise Designed and Implemented to Supplement the Teaching of Biochemical Pathways
09:27

Functional Complementation Analysis FCA: A Laboratory Exercise Designed and Implemented to Supplement the Teaching of Biochemical Pathways

Published on: June 24, 2016

17.6K

Action of the Terminal Complement Pathway on Cell Membranes.

Bill H T Ho1, Bradley A Spicer1, Michelle A Dunstone2

  • 1Monash Biomedicine Discovery Institute, Department of Biochemistry and Molecular Biology, Monash University, Melbourne, VIC, Australia.

The Journal of Membrane Biology
|March 24, 2025
PubMed
Summary
This summary is machine-generated.

The complement system

Keywords:
AnaphylatoxinC5a receptorCell membranesComplement systemInflammationMembrane attack complexRegulationTerminal complement pathway

More Related Videos

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

7.4K
Targeting Cysteine Thiols for in Vitro Site-specific Glycosylation of Recombinant Proteins
11:25

Targeting Cysteine Thiols for in Vitro Site-specific Glycosylation of Recombinant Proteins

Published on: October 4, 2017

6.5K

Related Experiment Videos

Last Updated: May 20, 2025

Functional Complementation Analysis FCA: A Laboratory Exercise Designed and Implemented to Supplement the Teaching of Biochemical Pathways
09:27

Functional Complementation Analysis FCA: A Laboratory Exercise Designed and Implemented to Supplement the Teaching of Biochemical Pathways

Published on: June 24, 2016

17.6K
Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

7.4K
Targeting Cysteine Thiols for in Vitro Site-specific Glycosylation of Recombinant Proteins
11:25

Targeting Cysteine Thiols for in Vitro Site-specific Glycosylation of Recombinant Proteins

Published on: October 4, 2017

6.5K

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • The complement pathway is a crucial part of innate immunity, targeting pathogens.
  • Late complement activation involves C5a receptors (C5aR1, C5aR2) and the Membrane Attack Complex (MAC).
  • Host cells possess inhibitors like clusterin and CD59 to prevent complement-mediated damage.

Purpose of the Study:

  • To review recent molecular and structural insights into C5a receptor activation and MAC assembly regulation.
  • To explore the molecular basis of inflammatory diseases resulting from dysregulated terminal complement effectors.
  • To outline potential crosstalk between C5a receptor signaling and MAC-mediated responses.

Main Methods:

  • Literature review of molecular and structural studies.
  • Analysis of disease mechanisms linked to complement dysregulation.
  • Synthesis of information on C5a receptor and MAC pathways.

Main Results:

  • Recent advances in understanding C5a receptor (C5aR1, C5aR2) activation and modulation.
  • Insights into the regulation of Membrane Attack Complex (MAC) assembly.
  • Identification of shared inflammatory disease outcomes due to dysregulated terminal complement effectors.

Conclusions:

  • Dysregulation of terminal complement effectors, including C5a receptors and MAC, underlies inflammatory diseases.
  • Crosstalk and synergy between C5a receptor activation and MAC-mediated cellular responses contribute to disease pathogenesis.
  • Further research into these interactions may reveal novel therapeutic targets.