Catterall J F, Watson C S, Funkenstein B
Population Council, New York, NY 10021.
J Steroid Biochem. 1987;27(1-3):193-9. doi: 10.1016/0022-4731(87)90310-4.
The kidneys of androgen stimulated mice exhibit a hypertrophic response but no hyperplasia or concomitant DNA replication. Androgens increase the expression of several genes in mouse kidney. The response of the beta-glucuronidase gene to testosterone in this tissue is characterized by a 1-2 day lag and relatively slow induction kinetics. The gene coding for kidney androgen-regulated protein (KAP) exhibits quite a different response to the hormone when compared on the basis of initial response to a given dose, dose required to produce maximal response, and apparent sensitivity to low levels of androgen-receptor complexes in renal nuclei. The analysis of the accumulation of the mRNAs produced by these two genes suggests that gene-specific differential sensitivity to androgen receptor complexes governs the development of the cellular male phenotype in this tissue.
雄激素刺激的小鼠肾脏呈现肥大反应,但无增生或伴随的DNA复制。雄激素可增加小鼠肾脏中几种基因的表达。该组织中β-葡萄糖醛酸酶基因对睾酮的反应特点是有1-2天的延迟以及相对缓慢的诱导动力学。与基于对给定剂量的初始反应、产生最大反应所需剂量以及对肾细胞核中低水平雄激素受体复合物的明显敏感性相比,编码肾脏雄激素调节蛋白(KAP)的基因对该激素表现出截然不同的反应。对这两个基因产生的mRNA积累的分析表明,对雄激素受体复合物的基因特异性差异敏感性决定了该组织中细胞雄性表型的发育。