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results suggest that the C4B gene number associates positively with inflammation in patients with PIBD. Multiple copies of the C4B gene may thus aggravate the IBD-associated dysbiosis through escalated complement reactivity towards the microbiota.
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.
The structural basis for inhibition of the classical and lectin complement pathways by S. aureus extracellular adherence protein binding to C4b has been presented.
The aims of this study were to elucidate the copy number variations of C4A and C4B in relation to disease risk in systemic lupus erythematosus, and to compare the basis of race-specific C4A deficiency between East Asians and individuals of European descent
C4A and C4B gene copy numbers are stronger risk factors for juvenile-onset than for adult-onset systemic lupus erythematosus
Data indicate Ig-like transcript 4 (ILT4 (Montrer LILRB2 Protéines)) as a cellular receptor for complement split products (CSPs) complement component 4d (C4d).
Suggest a prominent prognostic value of C4d staining as a rejection marker in ABO compatible kidney transplantation.
The interaction between C4BP (Montrer C4BPA Protéines) and Leptospira interrogans LcpA, LigA and LigB is sensitive to ionic strength and inhibited by heparin.
There was a significant association between C4d deposition on allograft endothelial cells and presence of class II DSA I chronic liver allograft failure.
Carrying no copies of C4B significantly increases the risk of cCSC, whereas carrying three C4B copies is protective.
Data indicate complement C3 (Montrer C3 Protéines) deposition on peanut extract (PE) was abolished in immunoglobulin- and C4-deficient sera.
a deficiency in C4b does not alter radiation-induced lung disease in the C57BL/6 mouse model
C3 and C4 bind to collagen and elastin (Montrer ELN Protéines) in the vascular wall and have a potential role in vascular stiffness and atherosclerosis
Complement C4 provides an important protective role against the development of systemic lupus erythematosus.
identified the murine follicular dendritic cell marker, FDC-M2, as complement c4. FDC-M2 was detectable at sites of immune complex-mediated inflammatory disease
The increased mortality of C4(-/-) or Factor B (Montrer CFB Protéines)(-/-) mice indicates that these two pathways of complement activation are required for survival in mousepox.
Increased transcription of the complement C4 gene in the Rag1 (Montrer RAG1 Protéines)(-/-) intestine.
This gene encodes the basic 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. 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. In addition, this gene exists as a long form and a short form due to the presence or absence of a 6.4 kb endogenous HERV-K retrovirus in intron 9.
C3 and PZP-like alpha-2-macroglobulin domain-containing protein 3
, Chido form of C4
, basic complement C4
, complement C4-B
, complement C4B1a
, complement component 4A
, complement component 4B
, complement component 4B (Chido blood group)
, complement component 4 (within H-2S)
, complement component 4B (Childo blood group)
, complement C4-like protein
, complement component 4, gene 2