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anti-Human C1QA Antibodies:
anti-Rat (Rattus) C1QA Antibodies:
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Cow (Bovine) Polyclonal C1QA Primary Antibody for WB - ABIN6746748
Steegmaier, Yang, Yoo, Huang, Shen, Yu, Luo, Scheller: Three novel proteins of the syntaxin/SNAP-25 family. in The Journal of biological chemistry 1999
Show all 2 Pubmed References
Human Polyclonal C1QA Primary Antibody for WB - ABIN6137751
Deng, Xu, Fang, Yu, Zhu, Chen, Liu, Zhou: The Surface-Exposed Protein SntA Contributes to Complement Evasion in Zoonotic Streptococcus suis. in Frontiers in immunology 2018
the overall architecture of Dare-C1qAgD is similar to human C1qA, residues involved in C1qBgD, C1qCgD, and CRP binding are somewhat different while residues involved in IgG binding are not present in zebrafish. The structure gives insight into how human and fish C1qA evolved from an ancestral protein
C1qA globular domain (C1qAgD) was expressed, purified and crystallized.
This study demonstrated C1q levels were elevated in Polymyositis/Dermatomyositis patients with higher Erythrocyte Sedimentation Rate and revealed significant positive correlation.
Detection of complement binding activity using both C1q and C3d assays can be a further prognostic marker for predicting antibody mediated rejection and allograft outcome in donor-specific HLA antibodies kidney transplant patients.
These findings demonstrate that C1q and it's globular region interact with CD33 to activate its inhibitory motifs, while the collagen-like region does not. Whole C1q is required to crosslink CD33 and LAIR-1 and concurrently activate CD33/LAIR-1 inhibitory motifs.
this study shows that regulatory dendritic cells can mediate a potent direct anti-inflammatory activity via the expression and/or secretion of molecules such as C1q, independently of their capacity to expand the pool of regulatory T cells
analysis of molecular signaling and inflammatory responses during ingestion of atherogenic lipoproteins modulated by complement protein C1q
these data show that C1q is involved in the process of embryo implantation contributing to the remodeling of spiral arteries
Studies indicate that complement C1q (C1q) is a multifunctional homeostatic regulator in the central nervous system (CNS).
We, for the first time, identified the associations between C1q gene SNPs and autoimmune thyroid diseases, and our findings suggested that five common SNPs in C1q gene were not associated with autoimmune thyroid diseases susceptibility in Chinese Han population
exposure of neural stem cells to neutrophil-synthesized concentrations of C1q and C3a promoted astrogliogenesis and cell migration
Anti-C1q-induced C1q secretion might be an important immune-modulatory factor in systemic lupus erythematosus.
this studies show binding of VWF to C1q and thus a direct interaction between starter molecules of hemostasis and the classical pathway of complement
Cerebrospinal fluid (CSF) soluble complement receptor 2 (sCR2) levels correlated significantly both with CSF complements C3 and C1q as well as to a disease severity measure.
decreased levels result in predominant skin manifestations in children
anti-C1q induced a proinflammatory phenotype in human monocyte-derived macrophages reversing the effects of immobilized C1q alone
These findings support a role for locally synthesized C1q in promoting tumor growth.
This study reveled that C1QA having a central role in the bipolar disease and schizophrenia manifestation.
The A allele and AA genotype of C1q rs292001 can be considered a susceptibility risk factor and the GG genotype could be considered protective for juvenile systemic lupus erythematosus and lupus nephritis in the studied cohort of Egyptian children.
no significant association found to either rs15940 (C1QA) or rs172378 (C1QC) when analysed in just Parkinson disease cases , just controls or combined
Elevation in serum C1q levels are associated with sarcopenia.
Our findings showed that Brugia malayi Calreticulin (BmCRT) is responsible for the prevention of classical complement pathway activation via its interaction with the first component C1q of the human host
IgG3-antigen complexes are deposited on follicular dendritic cells in the presence of C1q and C3.
C1qa(-/-) mice did not show any differences in photoreceptor loss or inflammation at 7 days compared to wild-type
The results presented here demonstrate that the C1q expression in aged females experience a distinct difference in brain aging when compared to age-matched males, suggesting females undergo a higher level of microglial activation with age.
Data preliminarily suggest that complement C1q activity may aid in the clearance of the Toxoplasma gondii parasite from the central nervous system and in so doing, have consequences for the connectivity of neighboring cells and synapses
C1q-/- mice manifest increased frequency of fetal resorption, reduced fetal weight, and smaller litter size when compared to their wild-type counterparts
This study demonstrated that microglia, but not neurons or peripheral sources, are the dominant source of C1q in the brain.
findings show that C1q rather than FcgammaRs controls the Ab-mediated Ag uptake and its presentation by spleen APC subsets to T cells
Demonstrate local synthesis of complement proteins by both PDGFRbeta-positive pericytes and CD45-positive cells in kidney fibrosis.
Deleting C1qa gene significantly reduces synaptic pruning by Grn(-/-) microglia and mitigates neurodegeneration, behavioral phenotypes, and premature mortality in Grn(-/-) mice; results uncover a previously unrecognized role of progranulin in suppressing aberrant microglia activation during aging.
C1q level may be a surrogate of prediction marker representing neurodegenerative disease progress before developing behavioral impairment.
developmental mechanisms of C1qa may be re-engaged during injury response
that inhibition of C1 is sufficient to preserve dendritic and synaptic architecture
C1q is involved in the pristane-mediated enhanced inflammatory response to TLR7 stimulation.
C1q has a role in pulmonary vascular homeostasis and preventing injury to lung endothelium
Data (including data from studies in mutant mice) suggest exercise prevents age-related neurovascular decline, up-regulation of C1qa, and down-regulation of astrocytic Apoe; this preventive effect of exercise does not occur in Apoe-deficient mice.
critical role in activation of beta-catenin signalling in hypertensive arterial remodelling
This gene encodes a major constituent of the human complement subcomponent C1q. C1q associates with C1r and C1s in order to yield the first component of the serum complement system. Deficiency of C1q has been associated with lupus erythematosus and glomerulonephritis. C1q is composed of 18 polypeptide chains: six A-chains, six B-chains, and six C-chains. Each chain contains a collagen-like region located near the N terminus and a C-terminal globular region. The A-, B-, and C-chains are arranged in the order A-C-B on chromosome 1. This gene encodes the A-chain polypeptide of human complement subcomponent C1q.
complement component 1, q subcomponent, alpha polypeptide
, complement C1q subcomponent subunit A
, complement component 1, q subcomponent, A chain
, complement component C1q, A chain
, complement C1qA