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红白血病分化。红系特异性和非特异性δ-氨基-γ-酮戊酸合酶mRNA的独特反应。

Erythroleukemia differentiation. Distinctive responses of the erythroid-specific and the nonspecific delta-aminolevulinate synthase mRNA.

作者信息

Fujita H, Yamamoto M, Yamagami T, Hayashi N, Sassa S

机构信息

Rockefeller University Hospital, New York, New York 10021.

出版信息

J Biol Chem. 1991 Sep 15;266(26):17494-502.

PMID:1894633
Abstract

We have examined the levels of delta-aminolevulinate synthase (ALAS) mRNAs encoding the erythroid-specific (ALAS-E) and the nonspecific (ALAS-N) ALAS isozymes in murine Friend virus-transformed erythroleukemia (MEL) cells. Both ALAS-E and ALAS-N mRNAs were detected in a clone of dimethyl sulfoxide (Me2SO)-sensitive MEL cells, termed DS-19, without cross-hybridization. Untreated DS-19 cells contained approximately 10-fold more ALAS-E mRNA than ALAS-N mRNA. When DS-19 cells were treated with Me2SO or hemin, ALAS-N mRNA declined rapidly, which was followed by a marked increase in ALAS-E mRNA. Similarly, the immunoquantifiable ALAS-N protein decreased, while the ALAS-E protein increased upon Me2SO treatment. A clone of Me2SO-resistant cells, termed DR-1, which fails to undergo erythroid differentiation, was found to lack ALAS-E mRNA, whereas it showed significant induction responses of mRNAs for other heme pathway enzymes by Me2SO treatment. DR-1 cells contained a similar level of an erythroid-specific transcription factor, GATA-1, as did DS-19 cells, and had neither major deletion nor rearrangement of the ALAS-E gene. These findings indicate that the genes encoding the two ALAS isozymes are under separate controls and suggest that ALAS-E mRNA accumulation is responsible for increased heme synthesis in MEL cells undergoing erythroid differentiation.

摘要

我们检测了编码红细胞特异性(ALAS-E)和非特异性(ALAS-N)δ-氨基-γ-酮戊酸合酶(ALAS)同工酶的mRNA水平,这些mRNA存在于鼠类Friend病毒转化的红白血病(MEL)细胞中。在一个对二甲亚砜(Me2SO)敏感的MEL细胞克隆(称为DS-19)中检测到了ALAS-E和ALAS-N mRNA,且二者无交叉杂交现象。未经处理的DS-19细胞中,ALAS-E mRNA的含量比ALAS-N mRNA多大约10倍。当用Me2SO或血红素处理DS-19细胞时,ALAS-N mRNA迅速下降,随后ALAS-E mRNA显著增加。同样,经Me2SO处理后,免疫定量的ALAS-N蛋白减少,而ALAS-E蛋白增加。发现一个对Me2SO耐药的细胞克隆(称为DR-1),它不能进行红细胞分化,该克隆缺乏ALAS-E mRNA,而经Me2SO处理后,它对其他血红素途径酶的mRNA表现出明显的诱导反应。DR-1细胞中红细胞特异性转录因子GATA-1的水平与DS-19细胞相似,且ALAS-E基因既没有大的缺失也没有重排。这些发现表明,编码两种ALAS同工酶的基因受不同的调控,并提示ALAS-E mRNA的积累是MEL细胞在进行红细胞分化时血红素合成增加的原因。

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