Levenson C W, Shay N F, Hempe J M, Cousins R J
Food Science and Human Nutrition Department, University of Florida, Gainesville 32611.
J Nutr. 1994 Jan;124(1):13-7. doi: 10.1093/jn/124.1.13.
The cysteine-rich intestinal protein (CRIP) is a member of a superfamily of proteins containing the LIM motif (a double zinc finger) that has been shown to bind zinc. The role of zinc in the regulation of CRIP was examined in adult rats, cultured intestinal epithelial cells and in a transient transfection system. When adult male rats were fed diets with various amounts of zinc, the amount of ileal CRIP mRNA was only 19% lower in rats fed a zinc-deficient diet (1 mg Zn/kg) and was not different in the zinc-supplemented group (180 mg Zn/kg) compared with the zinc-adequate group (30 mg Zn/kg). In contrast, metallothionein mRNA levels were 76% lower and 80% greater than control levels in the zinc-deficient and zinc-supplemented groups, respectively. Using the chloramphenicol acetyltransferase (CAT) reporter gene, 5'-deletion products of the CRIP genomic promoter were tested for basal and zinc-induced CAT activity in transiently transfected IEC-6 cells. Treatment of the cells with zinc did not alter CAT activity of any construct. These results suggest that CRIP is not directly regulated by zinc in the intestine of rats.
富含半胱氨酸的肠道蛋白（CRIP）是包含LIM基序（双锌指）的蛋白质超家族的成员，该基序已被证明能结合锌。在成年大鼠、培养的肠上皮细胞和瞬时转染系统中研究了锌在CRIP调节中的作用。当成年雄性大鼠喂食含不同锌量的饮食时，与锌充足组（30 mg Zn/kg）相比，喂食缺锌饮食（1 mg Zn/kg）的大鼠回肠CRIP mRNA量仅低19%，而锌补充组（180 mg Zn/kg）则无差异。相反，在缺锌组和锌补充组中，金属硫蛋白mRNA水平分别比对照水平低76%和高80%。使用氯霉素乙酰转移酶（CAT）报告基因，在瞬时转染的IEC-6细胞中测试了CRIP基因组启动子的5'-缺失产物的基础和锌诱导的CAT活性。用锌处理细胞不会改变任何构建体的CAT活性。这些结果表明，在大鼠肠道中CRIP不受锌的直接调节。
