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Article: Molecular analysis of C3 allotypes in Chinese patients with immunoglobulin A nephropathy

TitleMolecular analysis of C3 allotypes in Chinese patients with immunoglobulin A nephropathy
Authors
Issue Date1994
Citation
American Journal of Kidney Diseases, 1994, v. 23 n. 4, p. 543-546 How to Cite?
AbstractThe third component of complement (C3) exists in two main allotypic forms, C3S and C3F. An increased frequency of the rarer C3F allele has been reported in several autoimmune conditions, including immunoglobulin A nephropathy (IgAN), in white patients. C3F is known to be rare in the Chinese population, but C3 allotypes have not been studied in Chinese patients with IgAN. The molecular basis of the S/F polymorphism has been established recently: a single base change at the DNA level encodes a single amino acid substitution in the protein. A second polymorphism, closely linked to the first, is defined by the monoclonal antibody HAV 4-1, and also is due to a single base change. These polymorphisms therefore can be analyzed at the DNA level. We have used the amplification refractory mutation system, a modification of the polymerase chain reaction, to analyze these two C3 polymorphisms on genomic DNA from 133 Hong Kong Chinese individuals: 54 patients with IgAN and 79 controls. No C3F alleles were present in either group: all individuals were homozygous C3S. Twenty-six patients were also allotyped for the HAV 4-1 polymorphism; all 26 were homozygous HAV 4-1 negative, as would be predicted from the close linkage of this allotype to C3S in other populations. These data indicate that C3F is not a susceptibility allele for IgAN in Hong Kong Chinese individuals, and confirm in a large DNA-based study the rarity of C3F in this population.
Persistent Identifierhttp://hdl.handle.net/10722/195328
ISSN
2015 Impact Factor: 6.269
2015 SCImago Journal Rankings: 2.313
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFinn, JE-
dc.contributor.authorLi, PKT-
dc.contributor.authorKar Neng Lai-
dc.contributor.authorMathieson, PW-
dc.date.accessioned2014-02-28T06:11:59Z-
dc.date.available2014-02-28T06:11:59Z-
dc.date.issued1994-
dc.identifier.citationAmerican Journal of Kidney Diseases, 1994, v. 23 n. 4, p. 543-546-
dc.identifier.issn0272-6386-
dc.identifier.urihttp://hdl.handle.net/10722/195328-
dc.description.abstractThe third component of complement (C3) exists in two main allotypic forms, C3S and C3F. An increased frequency of the rarer C3F allele has been reported in several autoimmune conditions, including immunoglobulin A nephropathy (IgAN), in white patients. C3F is known to be rare in the Chinese population, but C3 allotypes have not been studied in Chinese patients with IgAN. The molecular basis of the S/F polymorphism has been established recently: a single base change at the DNA level encodes a single amino acid substitution in the protein. A second polymorphism, closely linked to the first, is defined by the monoclonal antibody HAV 4-1, and also is due to a single base change. These polymorphisms therefore can be analyzed at the DNA level. We have used the amplification refractory mutation system, a modification of the polymerase chain reaction, to analyze these two C3 polymorphisms on genomic DNA from 133 Hong Kong Chinese individuals: 54 patients with IgAN and 79 controls. No C3F alleles were present in either group: all individuals were homozygous C3S. Twenty-six patients were also allotyped for the HAV 4-1 polymorphism; all 26 were homozygous HAV 4-1 negative, as would be predicted from the close linkage of this allotype to C3S in other populations. These data indicate that C3F is not a susceptibility allele for IgAN in Hong Kong Chinese individuals, and confirm in a large DNA-based study the rarity of C3F in this population.-
dc.languageeng-
dc.relation.ispartofAmerican Journal of Kidney Diseases-
dc.titleMolecular analysis of C3 allotypes in Chinese patients with immunoglobulin A nephropathy-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0272-6386(12)80376-3-
dc.identifier.pmid8154490-
dc.identifier.scopuseid_2-s2.0-0028333634-
dc.identifier.volume23-
dc.identifier.issue4-
dc.identifier.spage543-
dc.identifier.epage546-
dc.identifier.isiWOS:A1994NF03400008-

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