一个常染色体显性基因调控小鼠红细胞唾液酸9 - O - 乙酰化的程度。这可能是激活人类替代补体途径能力存在差异的一种解释。
An autosomal dominant gene regulates the extent of 9-O-acetylation of murine erythrocyte sialic acids. A probable explanation for the variation in capacity to activate the human alternate complement pathway.
作者信息
Varki A, Kornfeld S
出版信息
J Exp Med. 1980 Sep 1;152(3):532-44. doi: 10.1084/jem.152.3.532.
Abstract
Nydegger et al. (4) have reported that the difference in susceptibility of erythrocytes from different inbred murine strains to lysis by the human alternate complement pathway is determined by an autosomal locus. We have found a good correlation between the degree of O-acetylation of the erythrocyte sialic acid residues and the susceptibility to complement lysis, whereas there was no correlation between total erythrocyte sialic acid content and complement sensitivity. The major O-acetylated species in all the murine strains is 9-O-acetyl-N-acetylneuraminic acid. We propose that the autosomal dominant locus, which determines complement sensitivity, acts by influencing the extent of 9-O-acetylation of the erythrocyte sialic acid residues. By using recombinant inbred strains, we determined that this genetic locus is probably located on chromosome 9. The nature of the gene product remains unknown.
摘要
尼德格等人（4）报告称，不同近交系小鼠品系的红细胞对人替代补体途径裂解的敏感性差异由一个常染色体位点决定。我们发现红细胞唾液酸残基的O-乙酰化程度与补体裂解敏感性之间存在良好的相关性，而红细胞总唾液酸含量与补体敏感性之间没有相关性。所有小鼠品系中的主要O-乙酰化物种是9-O-乙酰-N-乙酰神经氨酸。我们提出，决定补体敏感性的常染色体显性位点通过影响红细胞唾液酸残基的9-O-乙酰化程度起作用。通过使用重组近交系，我们确定该基因位点可能位于9号染色体上。基因产物的性质仍然未知。
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Autosomal locus regulates inverse relationship between sialic acid content and capacity of mouse erythrocytes to activate human alternative complement pathway.常染色体位点调节小鼠红细胞唾液酸含量与激活人类替代补体途径能力之间的反比关系。
Proc Natl Acad Sci U S A. 1978 Dec;75(12):6078-82. doi: 10.1073/pnas.75.12.6078.
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