抗μ抗体抑制脂多糖驱动的B细胞分化的机制。转录反式作用阻遏物的证据。
Mechanism of suppression of lipopolysaccharide-driven B cell differentiation by anti-mu antibodies. Evidence for a trans-acting repressor of transcription.
作者信息
Flahart R E, Lawton A R
机构信息
Department of Microbiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.
出版信息
J Exp Med. 1987 Oct 1;166(4):864-73. doi: 10.1084/jem.166.4.864.
Abstract
Bivalent anti-mu antibodies suppress LPS-driven B cell differentiation by inhibiting the coordinate activation of a family of differentiation-related genes, including those encoding the heavy, light, and J chains of IgM. We have shown that the presence of inhibitors of RNA or protein synthesis during a pulse with anti-mu can interfere with induction of suppression. We suggest that suppression is mediated by a trans-acting repressor protein with specificity for common motifs in regulatory regions of each of these genes.
摘要
双价抗μ抗体通过抑制包括编码IgM重链、轻链和J链的基因在内的一系列分化相关基因的协同激活，来抑制脂多糖驱动的B细胞分化。我们已经表明，在抗μ脉冲期间RNA或蛋白质合成抑制剂的存在会干扰抑制的诱导。我们认为抑制作用是由一种反式作用阻遏蛋白介导的，该蛋白对这些基因每个基因调控区域中的共同基序具有特异性。
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Mechanism of suppression of lipopolysaccharide-driven B cell differentiation by anti-mu antibodies. Evidence for a trans-acting repressor of transcription.抗μ抗体抑制脂多糖驱动的B细胞分化的机制。转录反式作用阻遏物的证据。
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