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Related Concept Videos

GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
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GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
Inhibition of Cdk Activity02:34

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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Drugs Acting on Autonomic Ganglia: Blockers

Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:

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Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
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Inhibiting the C5-C5a receptor axis.

Trent M Woodruff1, Kutty S Nandakumar, Francesco Tedesco

  • 1School of Biomedical Sciences, University of Queensland, St Lucia, QLD 4072, Australia. t.woodruff@uq.edu.au

Molecular Immunology
|May 10, 2011
PubMed
Summary

The complement system

Area of Science:

  • Immunology and Molecular Medicine
  • Complement System Biology
  • Drug Development and Therapeutics

Background:

  • Complement system activation drives inflammation in many diseases.
  • Cleavage of C5 generates C5a and C5b-9, key inflammatory mediators.
  • C5a and C5b-9 contribute to diseases like PNH, RA, and neurodegeneration.

Purpose of the Study:

  • To review methods for inhibiting C5a and C5b-9 generation and C5a signaling.
  • To analyze therapeutic strategies targeting the C5-C5a receptor axis.
  • To discuss current and emerging drugs for complement-mediated diseases.

Main Methods:

  • Comprehensive literature review of complement inhibition strategies.
  • Analysis of drug candidates targeting C5 cleavage or C5a activity.

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  • Examination of clinical trial data for complement inhibitors.

    • Main Results:

    • Multiple strategies exist to inhibit C5a and C5b-9 generation and signaling.
    • Targeting the C5-C5a axis shows promise for treating inflammatory diseases.
    • Eculizumab is the only approved drug, but numerous candidates are in trials.

    Conclusions:

    • The C5-C5a axis is a highly promising therapeutic target.
    • Inhibiting complement activation offers potential for treating intractable diseases.
    • Emerging drug candidates may expand treatment options for complement-mediated conditions.