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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Complement component 1, q subcomponent, B chain

complement protein involved in innate immune response [RGD, Feb 2006] (from NCBI)
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Top mentioned proteins: C1qa, POLYMERASE, HAD, CAN, CIs
Papers on C1qB
Identification of novel gene and pathway targets for human epilepsy treatment.
Wei et al., Jilin, China. In Biol Res, Dec 2015
In down-co-expression module, C1QB (complement C1s), C1S (complement component 1, S subcomponent) and CFI (complement factor I) were enriched in GO:0006955 ~ immune response.
Variation in complement protein C1q is not a major contributor to cognitive impairment in Parkinson's disease.
Hudson et al., Newcastle upon Tyne, United Kingdom. In Neurosci Lett, Jun 2015
Given the links between C1q and cognitive function we assessed the genetic variability of the C1q encoding genes: C1QA, C1QB and C1QC between PD patients and matched controls.
Differential expression of brain immune genes and schizophrenia-related behavior in C57BL/6N and DBA/2J female mice.
Tian et al., Helsinki, Finland. In Psychiatry Res, Apr 2015
The mRNA levels of Il1b and Il6 genes were significantly higher in the cortex and hypothalamus, while the mRNA level of C1qb was lower in the cortex, hippocampus and hypothalamus of DBA/2J mice compared to C57BL/6N mice.
Molecular characterization of the complement C1q, C2 and C4 genes in Brazilian patients with juvenile systemic lupus erythematosus.
Carneiro-Sampaio et al., São Paulo, Brazil. In Clinics (sao Paulo), Mar 2015
C1qB mRNA expression was decreased compared with that of controls and did not change with stimulation.
Renal C3 complement component: feed forward to diabetic kidney disease.
Dominguez et al., Indianapolis, United States. In Am J Nephrol, 2014
The classic complement pathway was activated in diabetic kidneys with significant increases of C1qa, C1qb, and C1qc mRNAs in DI over LS.
Characterising the immune profile of the kidney biopsy at lupus nephritis flare differentiates early treatment responders from non-responders.
Rovin et al., Columbus, United States. In Lupus Sci Med, 2014
The top genes responsible for CR clustering included several interferon pathway genes (STAT1, IRF1, IRF7, MX1, STAT2, JAK2), while complement genes (C1R, C1QB, C6, C9, C5, MASP2) were mainly responsible for NR clustering.
The HLA-B*35 allele modulates ER stress, inflammation and proliferation in PBMCs from Limited Cutaneous Systemic Sclerosis patients.
Trojanowska et al., Boston, United States. In Arthritis Res Ther, 2014
Among genes downregulated by HLA-B*35 lentivirus were genes related to complement (C1QB, C1QC), cell cycle (CDNK1A) and apoptosis (Bax, Gadd45).
Bioinformatics Analysis of Potential Candidates for Therapy of TDRD7 Deficiency-Induced Congenital Cataract.
Wang et al., Beijing, China. In Ophthalmic Res, 2014
In the PPI network, high-degree genes of complement component 1, q subcomponent, A/B/C chain (C1QA/C1QB/C1QC), lymphocyte antigen 86 (LY86) and neuroblastoma RAS viral oncogene homolog (NRAS) were identified.
Association of brain immune genes with social behavior of inbred mouse strains.
Tian et al., Helsinki, Finland. In J Neuroinflammation, 2014
The mRNA levels of H2-d1 in the prefrontal cortex, hippocampus, and hypothalamus and C1qb in the hippocampus of the DBA/2 J strain were significantly down-regulated as compared to those in the C57BL/6 J strain.
Activated complement classical pathway in a murine model of oxygen-induced retinopathy.
Lei et al., Chongqing, China. In Int J Ophthalmol, 2014
The expressions of C1qb and C4b genes in the OIR retina were significantly higher than those of the controls.
Systematic identification of trans eQTLs as putative drivers of known disease associations.
Franke et al., Groningen, Netherlands. In Nat Genet, 2013
Some of these SNPs affect multiple genes in trans that are known to be altered in individuals with disease: rs4917014, previously associated with systemic lupus erythematosus (SLE), altered gene expression of C1QB and five type I interferon response genes, both hallmarks of SLE.
[Research advances in the Cap gene of circovirus and its encoding capsid protein].
Jia et al., Chengdu, China. In Bing Du Xue Bao, 2013
This review summarizes the research advance of Cap gene of circovirus in the sequence characteristics, its encoding capsid protein, basic functions of the capsid protein and its interaction with MKRN1 protein, Hsp40 protein, receptor protein gClqR and complement factor C1qB protein.
Molecular mechanisms for synchronized transcription of three complement C1q subunit genes in dendritic cells and macrophages.
Lu et al., Singapore, Singapore. In J Biol Chem, 2011
analysis of the molecular mechanisms for synchronized transcription of three complement C1q subunit genes (A, B and C) in dendritic cells and macrophages
Transcriptome profiling of whole blood cells identifies PLEK2 and C1QB in human melanoma.
Fujita et al., Aurora, United States. In Plos One, 2010
a 2-gene signature consisting of PLEK2 and C1QB led to the best result that correctly classified 93.3% melanoma patients and 90% healthy controls
Association of C1QB gene polymorphism with schizophrenia in Armenian population.
Petrek et al., Yerevan, Armenia. In Bmc Med Genet, 2010
The susceptibility for schizophrenia was particularly associated with C1QB rs291982 GG genotype.
Assessing association of common variation in the C1Q gene cluster with systemic lupus erythematosus.
Eggleton et al., Exeter, United Kingdom. In Clin Exp Immunol, 2010
In a large family-based association study of C1Q gene cluster polymorphisms no evidence for a genetic role of C1Q locus SNP in systemic lupus erythematosus risk predisposition was obtained in patients of European ancestry.
Complement component C3 binds to activated normal platelets without preceding proteolytic activation and promotes binding to complement receptor 1.
Nilsson et al., Uppsala, Sweden. In J Immunol, 2010
Data show that C1q, C4, C3, and C9 bind to thrombin receptor-activating peptide-activated platelets in lepirudin-anticoagulated platelet-rich plasma (PRP) and whole blood.
PPAR-delta senses and orchestrates clearance of apoptotic cells to promote tolerance.
Chawla et al., Stanford, United States. In Nat Med, 2009
Genetic deletion of PPAR-delta decreases expression of opsonins such as complement component-1qb (C1qb), resulting in impairment of apoptotic cell clearance and reduction in anti-inflammatory cytokine production.
Systems biology approach predicts immunogenicity of the yellow fever vaccine in humans.
Pulendran et al., Atlanta, United States. In Nat Immunol, 2009
Computational analyses identified a gene signature, including complement protein C1qB and eukaryotic translation initiation factor 2 alpha kinase 4-an orchestrator of the integrated stress response-that correlated with and predicted YF-17D CD8(+) T cell responses with up to 90% accuracy in an independent, blinded trial.
Complement factors in adult peripheral nerve: a potential role in energy metabolism.
Lemke et al., Los Angeles, United States. In Neurochem Int, 2004
Here we show that components of both the classical (C1qa, C1qb, C1qc, C2 and C4) and alternative (C3, B and adipsin) pathways are expressed by uninjured peripheral nerve as well.
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