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Título

A physical map of the human regulator of complement activation gene cluster linking the complement genes CR1, CR2, DAF, and C4BP

AutorRey-Campos, J.; Rubinstein, Pablo; Rodríguez de Córdoba, Santiago
Fecha de publicación1-feb-1988
EditorRockefeller University Press
CitaciónJ Exp Med. 1988,167(2):664-9.
ResumenThe human genes encoding the regulatory complement components C4-binding protein (C4BP), the Cab/C4b receptor (CR1), the decay-accelerating factor (DAF), and factor H (H) are linked and define the regulator of complement activation (RCA) gene cluster (1-3), which maps to band q32 of chromosome 1 (4, 5). The same chromosomal location has been reported for the human gene encoding the C3dg receptor (CR2) (4), suggesting that CR2 also belongs to this linkage group. Since the RCA gene cluster encodes the proteins involved in the control of the C3-convertases (reviewed in reference 6), it represents the regulatory counterpart of the class III gene cluster of the MHC that encodes the structural components of the C3-convertases C2, B, and C4 (reviewed in reference 7). In spite of their nonsyntenic chromosomal location, the functionally related MHC-class III and RCA gene clusters may share a common evolutionary history. They encode proteins that bind to C3b and/or C4b and share a particular structural organization ofrepeats of60 amino acids characterized by a framework of highly conserved residues (reviewed in reference 8) . Early attempts to determine the genetic organization of the RCA cluster have separated the H gene from the CR1, C4BP, andDAFgenes (9), but the lack of recombinations between the latter has not allowed a more detailed map to emerge from formal genetic analyses . This difficulty has now been overcome through the analysis of very large genomic DNA fragments using pulsed field gel electrophoresis (PFGE) and we have aligned the CR1, CR2, DAF, and C4BP genes on an 800-kb DNA segment .
Descripción6 p.-2 fig.
Versión del editorhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2188826/
URIhttp://hdl.handle.net/10261/115516
ISSN0022-1007
E-ISSN1540-9538
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