Path: /proteins/c1qc-protein
Title: C1QC Protein (C1q Gamma Chain)
Tags: section:proteins, kind:protein
| C1QC Protein (C1q Gamma Chain) |
|---|
| Gene | [C1QC](/genes/c1qc) |
| UniProt ID | [P02747](https://www.uniprot.org/uniprot/P02747) |
| PDB Structures | 1C2B, 1PK6 |
| Molecular Weight | ~26 kDa |
| Subcellular Localization | Secreted, extracellular space |
| Protein Family | C1q family, [complement system](/entities/complement-system) |
| Length | 245 amino acids |
| Associated Diseases | Systemic lupus erythematosus, Alzheimer's disease, age-related macular degeneration |
C1QC (Complement component 1, q subcomponent, C chain) is a 245-amino acid protein that forms part of the C1q molecule, the recognition component of the classical complement pathway. C1q is a multimeric protein composed of six A, six B, and six C chains.
C1QC has a unique structure:
- C1q domain: C-terminal globular domain (gC1q) responsible for target recognition
- N-terminal collagen-like region: Forms the stalk of the molecule
- Disulfide bonds: Stabilize the trimeric structure
- Hexameric assembly: Six A-B-C heterotrimers form the complete C1q molecule
The globular domains recognize patterns on apoptotic cells, pathogens, and immune complexes.
C1q performs essential functions in innate immunity:
- Pattern recognition: Binds to pathogen-associated molecular patterns (PAMPs)
- Apoptotic cell clearance: Recognizes phosphatidylserine on dying cells
- Immune complex handling: Binds to antibody-antigen complexes
- Complement activation: Initiates the classical complement cascade
- Synaptic pruning: Tags weak synapses for elimination during development
C1q contributes to neuroinflammation in AD:
- C1q binding to Aβ promotes complement activation
- Synaptic elimination by microglia may contribute to synapse loss
- Increased C1q expression in AD brains
- Therapeutic targeting of C1q to reduce neuroinflammation under investigation
C1q plays a role in AMD pathogenesis:
- Drusen formation involves complement components
- C1q polymorphisms associated with AMD risk
- RPE cell damage from complement-mediated inflammation
C1q contributes to demyelination:
- Complement-mediated oligodendrocyte death
- Blood-brain barrier breakdown
- Therapeutic complement inhibitors in clinical trials
- Anti-C1q antibodies to block complement-mediated damage
- Small molecule inhibitors of C1q function
- CRISPR-based approaches to modulate C1q expression
- Complement inhibitors (e.g., eculizumab) being tested in neurodegenerative conditions
- Kishore et al., C1q family: structure and functions (2004)
- Bohlson et al., C1q in innate immunity (2014)
- Hong et al., C1q and Alzheimer's disease (2016)
- Stephan et al., C1q and synaptic pruning (2016)