Metallothionein mRNA expression in mice homozygous for chromosomal deletions around the albino locus.

Metallothionein mRNA expression in mice homozygous for chromosomal deletions around the albino locus.
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白化基因座周围染色体缺失的纯合小鼠中金属硫蛋白 mRNA 的表达。

DOI:
10.1073/pnas.85.4.1161
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发表时间:
1988
影响因子:
11.1
通讯作者:
Gluecksohn-Waelsch,S
Gluecksohn-Waelsch,S
中科院分区:
综合性期刊1区
文献类型:
--
作者:
DeFranco,D;MorrisJr,SM;Leonard,CM;Gluecksohn-Waelsch,S

文献摘要

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相似文献

小鼠7号染色体的缺失影响金属硫蛋白基因Mt-1的表达,其定位在8号染色体上,并且在c3 H或c14 CoS缺失纯合子的新生小鼠肝脏中Mt-1 mRNA的稳态水平降低至正常水平的15-40%。糖皮质激素不能诱导肝MT-1 mRNA水平的缺失纯合子,在正常的窝。然而,氯化锌是有效的诱导缺失纯合子以及他们的正常同窝仔的肝脏中的MT-1 mRNA水平。其他组织(例如,肾和肠)的缺失纯合子表达的Mt-1 mRNA的基础水平高于正常同窝出生的那些。在肠道中,这些还可由激素和金属剂诱导。因此,缺失纯合子中Mt-1基因的诱导缺失仅涉及糖皮质激素,并且还限于特定的细胞类型(即,肝细胞)。通常在7号染色体缺失区编码的反式作用因子似乎有助于赋予肝细胞中的金属硫蛋白基因对激素诱导信号作出反应的基本能力。
Deletions in chromosome 7 of the mouse affect the expression of the metallothionein gene Mt-1, which maps on chromosome 8, and steady-state levels of Mt-1 mRNA are reduced to 15-40% of normal in livers of newborn mice homozygous for either the c3H or c14CoS deletion. Glucocorticoids fail to induce hepatic Mt-1 mRNA levels in deletion homozygotes in contrast to normal littermates. However, zinc chloride is effective in inducing Mt-1 mRNA levels in livers of deletion homozygotes as well as of their normal littermates. Other tissues (e.g., kidney and intestine) of deletion homozygotes express basal levels of Mt-1 mRNA higher than those of normal littermates. In the intestine these are furthermore inducible by both hormonal and metal agents. Thus, loss of inducibility of the Mt-1 gene in deletion homozygotes concerns glucocorticoids only and is furthermore restricted to specific cell types (i.e., hepatocytes). The trans-acting factor(s) normally encoded in the deleted region of chromosome 7 appears to be instrumental in conferring on the metallothionein gene in hepatocytes the essential competence to respond to hormonal inducing signals.