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anti-Human C4A Antikörper:
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Human Polyclonal C4A Primary Antibody für WB - ABIN5693263
Wang, Zhang, Wang, An: Complement activity in the egg cytosol of zebrafish Danio rerio: evidence for the defense role of maternal complement components. in PLoS ONE 2008
Show all 2 Pubmed References
This reported cohort of homozygous deficiencies of C4A or C4B suggests that C4 deficiencies may have various unrecorded disease associations.
Increased C4A RNA expression (which is associated with increased SZ risk) is associated with poorer memory function in patients with SZ and in healthy participants.
Patients with decreased complement C3/complement C4 (C3/C4) ratios displayed significantly more severe clinical characteristics and renal pathological features.
Aspergillus fumigatus conidial metalloprotease Mep1p cleaves host major complement components C3, C4, and C5.
C4A GCN (gene copy numbers) positively correlated with neuropil contraction in the dorsolateral prefrontal cortex and thalamus. Thus, C4A and C4B GCN are associated with neuropil contraction in regions often associated with schizophrenia, and may be neuromaturationally dependent.
Increased expression of C4A is associated with genetic risk for schizophrenia.
The purpose of this study was to evaluate C4A and C4B in patients with congenital adrenal hyperplasia in relation to CYP21A2 genotype and psychiatric and autoimmune comorbidity. We determined the copy numbers of C4A and C4B in 145 patients with CAH .No association was found between C4 copy number and autoimmune disease.
Low C4 in systemic lupus erythematosus patients is due to consumption rather than deficient synthesis related to lower C4A & B gene copy numbers.
Report strong association of systemic lupus erythematosus in individuals with low copy numbers of C4 and in particular in patients with complete deficiency of C4A.
An increase in serum C4, as wall as a decrease in C3, was an important outcome determinant for patients with immunoglobulin A nephropathy.
for the first time, a complete overview of C4 in SLE from genetic variation to binding capacity using a novel test. As this test detects crossing over of Rodgers and Chido antigens, it will allow for more accurate measurement of C4 in future studies.
The study re-evaluates low-resolution crystal structures of C4 via interactive molecular-dynamics flexible fitting. In terms of biology, the results provide a better structural framework for understanding the pivotal function of the C4 protein within the complement system.
An elevated number of C4 genes was observed in Alzheimer's disease (AD) patients as compared with healthy controls. The presence of high C4A and C4B copy numbers in AD patients could explain the increased C4 protein expression observed in AD patients, thus highlighting a possible role for C4A and C4B copy number variations in the risk of developing AD.
This study shows that the C4c/C4 ratio seems to be a better diagnostic measure than total antigenic C4 alone. Our findings underline that screening with total antigenic C4 implies a risk of overlooking C1-INH-HAE patients.
In comparison with C4-intact patients, C4-deficient patients had a different clinical/serologic lupus-like phenotype and lacked the lupus interferon signature.
C4 copy number variations and deficiency of C4A both play an important role in the risk and manifestations of systemic lupus erythematosus in East Asian and European populations
Complement C4A deficiency appears to be an important factor for the genetic risk and pathogenesis of juvenile dermatomyositis, particularly in patients with a DR3-positive background.
Solution Structures of Complement C2 and Its C4 Complexes Propose Pathway-specific Mechanisms for Control and Activation of the Complement Proconvertases.
Coronary atherosclerosis is distinguished by serum C4 complement up-regulation and ceruloplasmin down-regulation.
find strong statistical significance for association of increased copy number of C4A (OR 0.81 (0.73; 0.89);P = 4.4 x 10(-5)), with the effect most pronounced in individuals over 78 years (OR 0.67 (0.55; 0.81)) and females
C4 mediated synapse elimination during postnatal development
multiple mechanisms of male-specific gene expression
This gene encodes the acidic form of complement factor 4, part of the classical activation pathway. The protein is expressed as a single chain precursor which is proteolytically cleaved into a trimer of alpha, beta, and gamma chains prior to secretion. The trimer provides a surface for interaction between the antigen-antibody complex and other complement components. The alpha chain may be cleaved to release C4 anaphylatoxin, a mediator of local inflammation. Deficiency of this protein is associated with systemic lupus erythematosus and type I diabetes mellitus. This gene localizes to the major histocompatibility complex (MHC) class III region on chromosome 6. Varying haplotypes of this gene cluster exist, such that individuals may have 1, 2, or 3 copies of this gene. Two transcript variants encoding different isoforms have been found for this gene.
C3 and PZP-like alpha-2-macroglobulin domain-containing protein 2
, C4A anaphylatoxin
, Rodgers form of C4
, acidic C4
, acidic complement C4
, complement C4-A
, sex-limited protein
, complement C4
, complement component 4 (within H-2S)
, complement component 4, gene 1
, complement component 4B (Chido blood group)
, complement component 4B (Childo blood group)