Genetic regulation of mouse glycosylphosphatidylinositol-phospholipase D

被引：9
|
作者：
Flores-Borja, F
Kieszkievicz, J
Church, V
Francis-West, PH
Schofield, J
Rademacher, TW
Lund, T
机构：
[1] UCL, Dept Immunol & Mol Pathol, London W1T 4JF, England
[2] Kings Coll London, Dept Craniofacial Dev, London WC2R 2LS, England
来源：
BIOCHIMIE | 2004年 / 86卷 / 4-5期
关键词：
diabetes; NOD mouse; ApoA-I;
D O I：
10.1016/j.biochi.2004.04.003
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Glycosylphosphatidylinositol phospholipase D (GPI-PLD) has been proposed to be responsible for cleaving membrane-associated glycosylphosphatidyl inositol (GPI) molecules to generate inositol phosphoglycan (IPGs), which have growth factor-mimetic properties. We have cloned the mouse liver GPI-PLD cDNA, which has a sequence that differs from that previously isolated from a mouse glucagonoma cell library. Using a highly specific and very sensitive RNase protection assay, we found that the GPI-PLD expressed in adult/post-natal brain, antrum and insulin-producing cells is identical to that isolated from liver. The expression of mouse GPI-PLD in liver shows a complex genetic regulation with a mouse strain-specific variation. In addition, GPI-PLD mRNA levels were higher in 4-week old animals compared to older animals, and the GPI-PLD mRNA levels increased in mice that developed insulin dependent type 1 diabetes spontaneously. This suggests that the expression of liver GPI-PLD in mice is highly regulated. (C) 2004 Elsevier SAS. All rights reserved.
引用
收藏
页码：275 / 282
页数：8
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