上调基因-11(URG11)生物信息学与功能分析

应用基因芯片技术获取以稳定转染HBx基因的肝癌细胞Hep G(Hep G22-X)Y,以及非转染的肝癌细胞Hep G 2的差异表达基因,利用生物信息学方法对其进行初步分析表明,该蛋白基因编码673个氨基酸,预测分子量为17.06 k D,理论等电点为4.83,定位于细胞核,具有转录调控、生长因子、信号传导的功能,同源性分析结果表明,其碱基序列与已经报道的其他12个物种的相似率为76%-97%,且符合种属之间的进化关系。     

Molecular biology of 11β-hydroxylase and 11β-hydroxysteroid dehydrogenase enzymes

There are two steroid 11β-hydroxylase isozymes encoded by the CYP11B1 and CYP11B2 genes on human chromosome 8q. The first is expressed at high levels in the normal adrenal gland, has 11β-hydroxylase activity and is regulated by ACTH. Mutations in the corresponding gene cause congenital adrenal hyperplasia due to 11β-hydroxylase deficiency; thus, this isozyme is required for cortisol biosynthesis. The second isozyme is expressed at low levels in the normal adrenal gland but at higher levels in aldosterone-secreting tumors, and has 11β-hydroxylase, 18-hydroxylase and 18-oxidase activities. The corresponding gene is regulated by angiotensin II, and mutations in this gene are found in persons who are unable to synthesize aldosterone due to corticosterone methyloxidase II deficiency. Thus, this isozyme is required for aldosterone biosynthesis.

Cortisol and aldosterone are both effective ligands of the “mineralocorticoid” receptor in vitro, but only aldosterone is a potent mineralocorticoid in vivo. This apparent specificity occurs because 11β-hydroxysteroid dehydrogenase in the kidney converts cortisol to cortisone, which is not a ligand for the receptor. This enzyme is a “short-chain” dehydrogenase which is encoded by a single gene on human chromosome 1. It is possible that mutations in this gene cause a form of childhood hypertension called apparent mineralocorticoid excess, in which the mineralocorticoid receptor is not protected from high concentrations of cortisol.     

白细胞介素11的研究进展

白细胞介素１１是复杂的细胞因子网络中一种新的多功能调节因子。ＩＬ－１１对多种造血祖细胞具有刺激作用,不仅在调节骨髓造血方面具有多种功能,而且在宿主防御系统至关重要的免疫变化中也起着重要作用。本文介绍了ＩＬ－１１的基因结构及其主要生物学功能。