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Validated All-in-One™ qPCR Primer for C3(NM_000064.3) Search again
Product ID:
HQP110834
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
AHUS5, ARMD9, ASP, C3a, C3b, CPAMD1, HEL-S-62p
Gene Description:
complement C3
Target Gene Accession:
NM_000064.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
Complement component C3 plays a central role in the activation of complement system. Its activation is required for both classical and alternative complement activation pathways.
Gene References into function
- Allelic distribution of complement components BF, C4A, C4B, and C3 in Psoriasis vulgaris.
- complement interaction with trypanosomatid promastigotes in normal human serum
- genes of C3, hormone-sensitive lipase, and PPARgamma may exert a modifying effect on lipid and glucose metabolism in familial combined hyperlipidemia
- The postprandial plasma C3 response is impaired in familial combined hyperlipidemia patients, probably as a result of a delayed response by C3 (the precursor for the biologically active acylation-stimulating protein) acting on free fatty acid metabolism.
- results indicate that normal human hematopoietic stem and progenitor cells express functional C3aR and that the C3aR-C3a axis sensitizes the responses of these cells to SDF-1
- changes in acylation-stimulating protein and adiponectin are predictive of decreased apolipoprotein B and improved insulin action after gastric bypass surgery
- The physiological interaction between glycyrrhizin (GL) and serum C3, and the inhibitory effects of GL, & glycyrrhetinic acid on the phosphorylation of C3 by casein kinase 2
- C3bi binds to integrin alpha M beta 2
- C4b and C3b do not undergo the same conformational changes upon binding to the C4BP mutants as during the interaction with the wild type C4BP, which then results in an observed loss of the cofactor activity
- The analysis involved the data on nine polymorphic codominant loci: HP, GC, TF, PI, PGM1, GLO1, C3, ACP1, and ESD. The loci were selected by significance of differences in genotype frequencies between tuberculosis patients and healthy controls
- IL-1alpha, IFN-gamma, and the combination of IL-1beta with IL-6 or IFN-gamma specifically enhanced C3 secretion by HepG2 cells
- upon physiological inactivation, C3b2-IgG complexes retain dimeric inactivated C3b and C3dg, which allows bivalent binding to the corresponding complement receptors
- ASP significantly predicted postprandial plasma triglyceride and NEFA clearance and, based on lower ASP, women may be more ASP sensitive than men
- A premature termination codon in the C3 gene results in a lack of the protein in serum, correlating with acceleration of C3 mRNA decay in fibroblasts consistent with a nonsense-codon-mediated decay process.
- Expressed in a bacterial system, a recombinant C3 segment of C345C module has substantial beta-sheet structure and internal disulfide bonds but does not inhibit complement hemolytic activity, and does not bind C6 or C7.
- findings show a significant genetic contribution to variation in circulating levels of acylation-stimulating protein and an interesting pattern of genetic correlation (i.e., pleiotropy) with other risk factors associated with the metabolic syndrome
- electrostatic calculations provide global and site-specific explanations of the physical causes that underlie the ionic strength dependence of C3d-CR2 association
- HGF and IL-1ra adhesion-dependent release from human blood granulocytes and monocytes involves plasma IgG, complement C3 and beta2 integrin
- MT1-MMP cleaves complement C3b
- Transgenic mice expressing C3a/glial fibrillary acidic protein (GFAP) in the brain progress to severe experimental autoimmune encephalomyelitis during the chronic phase of the disease, with significant mortality compared with nontransgenic littermates.
- thermodynamic analysis of interaction of C3 with its inhibitor, compstatin
- complement C3 expression is regulated by the bile acid receptor FXR
- characterized the interaction between the first two short consensus repeats (SCR1-2) of complement receptor type 2 (CR2, CD21) and C3d
- the open V-shaped structures formed by CR2 SCR 1-2, both when free and when bound to C3d, are optimal for the formation of a tight two-domain interaction with its ligand C3d
- mapped the regions of C3 involved in conformational transition when hydrolyzed to C3(H2O)
- iC3b interferes with monocyte-derived dendritic cell differentiation and IL-12 and IL-10 production is mediated via an ERK MAPK-dependent mechanism
- determination of C5L2 as its receptor and the receptor's role in mediating acylation stimulating protein triglyceride stimulation
- C3 secretion induced by CD40L may represent a mechanism of amplification of tubulointerstitial damage associated with lymphocyte infiltration.
- Moraxella catarrhalis UspA1/A2 exert their actions by absorbing and neutralizing C3 from serum and restrain complement activation
- C3a increased the binding affinity of CXCL12 to human CXCR4(+)/C3aR(-), REH pro-B cells, which is compatible with a direct interaction between C3a and CXCL12
- crystal structures of native C3 and its final major proteolytic fragment C3c
- properdin has a role in the assembly of the alternative pathway C3 convertases of complement
- streptavidin-C3dg enhancement of BCR-induced [Ca2+]i responses required CD21 and CD19 expression and resulted in significantly enhanced CD19 and Lyn phosphorylation, with enhanced Lyn/CD19 associations
- C3 gene is a priority candidate controlling risk for asthma and allergic disease in the Barbados population of African descent.
- data cast new light on the mechanism of complement-mediated tissue injury in nonimmunological disorders
- The differential expression of the complement proteins provides potentially useful biomarkers as well as evidence for the involvement of inflammatory processes in the pathogenesis of ALS and PD.
- Complement C3a is continuously elevated in deep second-degree burned wounds in patients older than 60 years. (complement 3a)
- Mannan-binding lectin activates C3 and the alternative complement pathway without involvement of C2
- South Asians have elevated C3 & CRP levels; results suggest they have a greater level of chronic subclinical inflammation independent of family history of stroke; C3 is more likely to cluster with features of insulin resistance syndrome compared with CRP
- C3a is acutely elevated after human ischemic stroke, C5a shows delayed elevations 7 to 14 days after cerebral ischemia, and sC5b-9 is acutely depressed after stroke. (Complement 3a, c5a, and C5b-9)
- C3d was somewhat more predictive of margination than C4d in ABO-incompatible
- Results describe three distinct profiles of serum complement C4 proteins in pediatric systemic lupus erythematosus (SLE) patients, and show tight associations of complement C4 and C3 protein levels in SLE but not in healthy subjects.
- crystal structure of C3b; structural data indicate that the large conformational changes in the proteolytic activation and regulation of C3 take place mainly in the first conversion step, from C3 to C3b
- C3 split products inactivated C3b (iC3b) and C3a were elevated in serum, overlying ARPE-19 cells that had accumulated A2E and were irradiated to induce A2E photooxidation
- Studies on two products of nucleophile addition to C3 reveal a structural intermediate in activation, and a final product, in which the anaphylatoxin domain has undergone a remarkable movement through the macroglobulin ring
- data indicate that C5L2 can function as a positive modulator for both C5a- and C3a-anaphylatoxin-induced responses
- Increased plasma ASP levels at late gestation may further contribute to the hyperlipidemic state, shifting energy in the form of triglycerides to the rapidly growing fetus.
- Impairment of the mechanisms involved in the regulation of activation of complement system factor C3c fragment may be important in the pathogenesis of endometriosis and endometriosis-associated infertility.
- in stenotic aortic valves, complement is activated leading to generation of the anaphylatoxin C3a
- These results indicate that C3 causes mesangial cells to convert to the synthetic phenotype and stimulates growth of mesangial cells, suggesting that C3 may play an important role in phenotypic regulation of mesangial cells in renal diseases.
- The common functional polymorphism rs2230199 (Arg80Gly) in the C3 gene, corresponding to the electrophoretic variants C3S (slow) and C3F (fast), was strongly associated with age-related macular degeneration in both English group and the Scottish group
- compstatin sterically hinders the access of the substrate C3 to the convertase complexes, thus blocking complement activation and amplification
- inflammatory processes involving C3a may contribute to delayed morbidity and mortality after aneurysmal rupture
- Identification of a nonsynonymous coding change in complement factor 3 that is strongly associated with risk of age-related macular degeneration in a large case-control sample.
- C3a and C5a can bring about eosinophil extravasation and increase in vascular permeability that facilitates eosinophil accumulation at sites of allergic inflammation.
- The dominant types of C1q complexes that circulate in vivo are C1q-C3d and C1q-C4d complexes.
- These results provide evidence for a novel role of C3 as a critical cofactor in human dendritic cell differentiation and maturation.
- C3 gene is associated with systemic lupus erythematosus and decreased serum level of C3 arre correlated with this allele.
- Levels are increased in young women with polycystic ovary syndrome.
- morphine modulates IL-1beta-mediated C3 expression in astrocytic cells.
- Results demonstrate alterations in C3 and ASP that may contribute to or compensate for dyslipidemia in pediatric proteinuric renal disease.
- Variation in C3 is associated with increased risk for age-related macular degeneration, with the R102G polymorphism showing the strongest evidence for the functional variant in our dataset.
- Maternal hypertriglyceridemia is associated with increased fetal ASP production, thus enhancing fetal fat storage independent of maternal glucose variations in nondiabetic women.
- Non-nuclear antibodies and C3 and C4 cluster within the families of SLE probands, suggesting that specific autoantibody formation is partly genetically determined, even if the total genetic effect in unaffected relatives is insufficient to cause disease
- Sbi helps mediate bacterial evasion of human complement C3 via a novel mechanism, namely futile fluid-phase consumption
- Hydrogen/deuterium exchange coupled with mass spectrometry (HDX-MS) is utilized to investigate relative changes in the solution-phase structures of C3 and C3b.
- study concluded that hyperglycaemia &/or hyperinsulinaemi per se regulated concentration & expression of leptin, adiponectin & acylation-stimulating protein in healthy lean young men, suggesting contribution to dysregulation of these hormones in diabetes
- C3 plays a beneficial role in plaque clearance and neuronal health as well as in modulation of the microglia phenotype in a complement C3-deficient amyloid precursor protein transgenic mouse model of Alzheimer's disease.
- Linkage disequilibrium block 4 spanning exons 24-41 of the C3 gene confers susceptibility to adult bronchial asthma, with mechanisms relevant to the effector phase of allergic inflammation in Japan.
- Report method for enzyme-independent, orientation-selective conjugation of whole human complement C3 to protein surfaces.
- A novel role for C3 that broadens its capacity to modulate acquired immune response.
- Polymorphisms within the C3 gene are associated with specific IgE levels to common allergens and super-antigens among atopic dermatitis patients
- C4BP binds to jeopardized cardiomyocytes early after acute myocardial infarct and co-localizes to other well known markers such as complemenb 3b.
- C3a is a highly sensitive early indicator of ischemia-reperfusion damage.
- study reports mutations in C3 in association with atypical hemolytic uremic syndrome (aHUS); 9 novel mutations in 14 aHUS patients with a persistently low serum C3 level are described
- Association of important functional defects of dendritic cells, acquisition of B cell memory, and regulatory T cells with C3 deficiency strongly supports a major role for C3 in bridging innate and adaptive immunity in humans.
- Changes in plasma adipokine ASP in early obesity are associated with blood lipid and glucose modifications, family environment, and distinct metabolic syndrome risk factors.
- analysis of denaturation and unfolding of human anaphylatoxin C3a
- Significantly more transcripts encoding alternative pathway components factor B, C3 and properdin, and C3a receptor and C5a receptor were detected in grade 3 versus grade 0 or 1 biopsies of human cardiac allografts.
- members of the Staphylococcus aureus extracellular fibrinogen-binding protein family inhibit the interaction of C3d with complement receptor 2
- during the menstrual cycle of normal women, the ASP levels coincidentally fluctuate with the progesterone levels, possibly reflecting cooperation between them in fat storage enhancement
- Sbi is a multifunctional bacterial protein, which binds host complement components Factor H and C3 as well as IgG and beta(2)-glycoprotein I and interferes with innate immune recognition.
- Our study showed a significant association between variants in the C3 gene and age-related macular degeneration (AMD) and further highlights the crucial role of the complement pathway in the etiology of AMD.
- The hazard ratios for allograft survival in the SS recipient and FS or FF donor group as compared with the other three groups were not significant
