| 2001 |
Bone marrow-derived cells (monocyte-macrophage lineage) are the source of serum C1q; transplantation of wild-type bone marrow into C1qa-/- mice fully reconstituted serum C1q levels within 6 weeks, while C1qa-/- bone marrow transferred into wild-type mice depleted C1q over 55 weeks. |
Bone marrow transplantation in C1qa-/- mice; serum C1q quantified by antigen assay and functional hemolytic assay; engraftment monitored by Y-chromosome PCR and genotype-specific PCR |
Journal of immunology |
High |
11564823
|
| 2017 |
Microglia, not neurons or peripheral sources, are the dominant source of C1q in the brain; conditional knockout of C1qa specifically in microglia (Cx3cr1-Cre) abolished C1q in the brain parenchyma without affecting plasma or peripheral organ C1q levels. |
Cell-type-specific conditional knockout (C1qa floxed x Cx3cr1-CreERT2); immunohistochemistry, qPCR, and western blot for C1q in brain, liver, kidney, and plasma |
Journal of neuroinflammation |
High |
28264694
|
| 1999 |
The cationic region comprising residues 14–26 of the C1qA polypeptide chain mediates C1q binding to anionic liposomes via electrostatic interactions; peptides containing this region (with ≥5 cationic residues) inhibited C1q binding to and complement activation by anionic liposomes in a charge-dependent, sequence-independent manner. |
Saturation binding assay with purified C1q and cardiolipin-containing liposomes; inhibition assays with synthetic C1qA14-26 peptides of varying charge; hemolytic complement activation assay |
Biochimica et biophysica acta |
High |
10209207
|
| 2009 |
Influenza A virus M1 matrix protein interacts with the globular region of C1qA through M1's N-terminal domain, blocking the interaction between C1qA and heat-aggregated IgG, inhibiting hemolysis, and preventing complement-mediated neutralization of influenza virus in vitro; in vivo, administered M1 promoted higher viral propagation and shortened survival of infected mice. |
Co-immunoprecipitation of M1 with C1qA; in vitro competition assay (M1 vs. heat-aggregated IgG for C1qA binding); hemolysis assay; neutralization assay; murine in vivo infection model with M1 administration |
The Journal of general virology |
Medium |
19656971
|
| 2012 |
C1qA interacts with components of the RIG-I/VISA signaling pathway and enhances RIG-I–VISA-mediated and TBK1-mediated activation of the IFN-β promoter; overexpression of C1qA upregulates RIG-I-mediated ISRE and NF-κB reporter activation and IFN-β transcription, but does not affect IRF3- or IKK-mediated ISRE/NF-κB activation; C1qA also counteracts the inhibitory function of the C1q receptor gC1qR in RIG-I-mediated signaling. |
Co-immunoprecipitation of C1qA with RIG-I pathway components; luciferase reporter assays for ISRE, NF-κB, and IFN-β promoters upon C1qA overexpression; functional comparison with gC1qR |
Immunology |
Medium |
22260551
|
| 2023 |
C1qA expression is regulated at the post-transcriptional level by METTL3-mediated m6A methylation; YTHDF2 acts as the m6A reader for C1qA mRNA; knockdown of METTL3 or YTHDF2 in Rituximab-resistant DLBCL cells upregulates C1qA expression, and restoring C1qA expression reduces Rituximab resistance both in vitro and in vivo. |
RNA immunoprecipitation with qPCR (RIP-qPCR); pulldown assays to identify METTL3 (writer) and YTHDF2 (reader); C1qA knockdown and overexpression in sensitive and resistant cell lines; in vitro CDC assays; xenograft mouse model |
Cell death discovery |
Medium |
37907575
|
| 2015 |
C1qa deletion in DBA/2NNia mice reduces retinal ganglion cell and optic nerve axonal loss in a sex-dependent manner (protective in males at 9–10 months, protective in females at 11–13 months), and decreases microglial activation in male mice at 5–6 months, establishing C1q as a mediator of complement-driven RGC damage in glaucoma. |
Congenic C1qa knockout mice in glaucoma model; retrograde labeling and semi-quantitative scoring of RGC and optic nerve; IOP measurement; microglial morphology assessment in flat-mounted retinas |
PloS one |
Medium |
26544197
|
| 2021 |
C1qa deficiency (CRISPR/Cas9 KO) enhances susceptibility to mouse hepatitis virus A59, resulting in more severe hepatocellular necrosis and interstitial pneumonia, higher viral loads in olfactory bulb, liver, and lungs, and dramatic elevations in splenic IFN-γ, MIP-1α, and MCP-1, demonstrating that classical complement pathway activation via C1qa is required for host protection against coronavirus infection. |
CRISPR/Cas9-generated C1qa KO mice; MHV-A59 infection model; histopathology; immunohistochemistry; quantitative viral load measurement; chemokine/cytokine quantification |
Journal of veterinary science |
Medium |
34056877
|
| 2024 |
In an AD mouse model (FAD4T), elevated C1qA protein and mRNA in activated microglia is associated with aberrant synaptic pruning leading to reduced dendritic spine density, decreased PSD-95 and NMDAR1 levels, and impaired miniature excitatory postsynaptic current amplitudes. |
RNA-seq; immunofluorescence; western blot; Golgi staining for dendritic spines; patch-clamp electrophysiology in hippocampal neurons |
Life sciences |
Low |
38266812
|
| 2024 |
C1qa knockout mice exhibit reduced hematoma erythrolysis, reduced neutrophil infiltration after intracerebral hemorrhage, but also delayed hematoma clearance associated with reduced induction of phagocytic multinuclear giant cells and increased perihematomal neuronal damage; after thrombin injection, C1qa KO mice had smaller lesion volumes, less neuronal loss, reduced neutrophil infiltration, and less BBB damage, indicating dual and context-dependent roles of C1qa in ICH-induced brain injury. |
C1qa KO mice; autologous blood injection and thrombin injection ICH models; MRI on days 1, 3, 7; immunohistochemistry for neutrophils, neurons, BBB markers, and phagocytic cells |
Translational stroke research |
Medium |
39370487
|
| 2024 |
NLRP12 forms a positive feedback loop with C1qA in tumor-associated macrophages (TAMs) to drive protumor M2-like polarization via the LILRB4/NF-κB pathway; NLRP12 knockout reversed macrophage polarization, enhanced T-cell anti-tumor immunity, and suppressed tumor growth in lung adenocarcinoma models. |
NLRP12 overexpression and knockdown in TAMs; NLRP12 KO mouse model; co-culture with tumor cells and T cells; NF-κB pathway analysis; tumor growth assays |
Cancer immunology, immunotherapy |
Low |
39527158
|
| 2032 |
Silencing C1QA in high-glucose-treated human renal tubular epithelial cells (HK-2) attenuated suppression of proliferation and reduced apoptosis, and concurrently downregulated endoplasmic reticulum stress effector proteins CHOP, XBP1s, and ATF6, indicating C1QA promotes HG-induced tubular epithelial injury by potentiating ERS. |
C1QA siRNA knockdown in HK-2 cells under high glucose conditions; CCK-8 viability assay; EdU proliferation assay; flow cytometry for apoptosis; western blot for ERS markers (CHOP, XBP1s, ATF6) |
Gene |
Medium |
42242331
|
| 2025 |
C1QA contributes to maintaining basal beta-catenin-dependent (norrin/FZD4) signaling in the retina; absence of C1QA in compound Tspan12 KO DBM; C1qa KO mice exacerbates blood-retina barrier dysfunction, cystoid edema, and neuroinflammation compared to Tspan12 KO DBM alone. |
Compound mutant mice (Tspan12 KO DBM; C1qa KO); BRB functional assays; MRI/imaging for cystoid edema assessment; ERG; microglia activation analysis; cell-based beta-catenin signaling assays |
bioRxivpreprint |
Medium |
bio_10.1101_2025.07.22.666172
|
| 2025 |
C1qA-deficient (C1qa KO) neonatal mice retain intersegmental proprioceptive Ia afferent connections at P11–13 that are normally eliminated by P11–13, phenocopying NaV1.6 conditional KO mice with impaired proprioceptor activity; NaV1.6 cKO mice show reduced C1qA expression in ventral spinal cord at P9, placing C1qA downstream of proprioceptor activity in complement-mediated elimination of excessive intersegmental synaptic connectivity. |
Ex vivo spinal cord electrophysiology in neonatal mice; C1qa KO and NaV1.6 cKO genetic models; immunostaining for C1qA expression; anatomical tracing of proprioceptive Ia afferents |
bioRxivpreprint |
Medium |
bio_10.1101_2025.08.22.671861
|