Folate deficiency reduces the GPI-anchored folate-binding protein in rat renal tubules.

Folate deficiency reduces the GPI-anchored folate-binding protein in rat renal tubules.
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叶酸缺乏会降低大鼠肾小管中 GPI 锚定的叶酸结合蛋白。

DOI:
10.1152/ajpcell.2000.278.4.c812
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发表时间:
2000
期刊:
American journal of physiology. Cell physiology
影响因子:
--
通讯作者:
Qian,L
Qian,L
中科院分区:
--
文献类型:
--
作者:
daCosta,M;Rothenberg,SP;Sadasivan,E;Regec,A;Qian,L

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叶酸结合蛋白(FBP)通过糖基磷脂酰肌醇(GPI)加合物锚定在细胞膜上,在一些转化和培养的细胞系中组成型表达。当这些细胞在含有低叶酸的培养基中生长时,其表达上调,但这是否发生在营养性叶酸缺乏的体内尚不清楚。为了解决这个问题,GPI-FBP在肝脏,肾脏和大脑的大鼠对照和叶酸缺乏(FD)饮食进行了测量。FD大鼠肾脏中GPI-FBP显著降低,而培养细胞中该蛋白表达上调。北方印迹分析和核运行试验表明,在肾脏中的GPI-FBP基因的转录没有减少叶酸缺乏。GPI-FBP的这种降低似乎是由其蛋白水解引起的,类似于体外发生的脱辅基蛋白的酶促降解。由于GPI-FBP位于近端肾小管的刷状缘上,并提供叶酸的重吸收,因此当叶酸缺乏时蛋白质减少时,该功能减弱。
A folate-binding protein (FBP) anchored to cell membranes by a glycosyl phosphatidylinositol (GPI) adduct is constitutively expressed in some transformed and cultured cell lines. Its expression is upregulated when these cells are grown in medium containing low folate, but whether this occurs in vivo with nutritional folate deficiency is unknown. To address this question, the GPI-FBP in the liver, kidney, and brain of rats on control and folate-deficient (FD) diets was measured. The GPI-FBP in the kidney of FD rats decreased significantly in contrast to the upregulation of this protein in cultured cells. Northern blot analysis and nuclear run-on assays indicated that transcription of the GPI-FBP gene in the kidney was not reduced by folate deficiency. This decrease of the GPI-FBP appears to result from its proteolysis, similar to the enzymatic degradation of the apoprotein that occurs in vitro. Because the GPI-FBP is on the brush borders of the proximal renal tubules and provides for the reabsorption of folate, this function diminishes when the protein decreases in folate deficiency.
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