The increase in levels of interferon-inducible proteins p202a and p202b and RNA-dependent protein kinase (PKR) during myoblast differentiation is due to transactivation by MyoD: their tissue distribution in uninfected mice does not depend on interferons.
The increase in levels of interferon-inducible proteins p202a and p202b and RNA-dependent protein kinase (PKR) during myoblast differentiation is due to transactivation by MyoD: their tissue distribution in uninfected mice does not depend on interferons.
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成肌细胞分化过程中干扰素诱导蛋白 p202a 和 p202b 以及 RNA 依赖性蛋白激酶 (PKR) 水平的增加是由于 MyoD 的反式激活：它们在未感染小鼠中的组织分布不依赖于干扰素。
DOI：
10.1089/10799900260100231
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Lengyel,P
中科院分区：
文献类型：
--
作者：
Wang,H;Ding,B;Liu,C-J;Ma,XY;Deschamps,S;Roe,BA;Lengyel,P
鼠200家族蛋白质p202 a、p202 b和p204以及RNA依赖性蛋白激酶（PKR）可由干扰素（IFN）诱导。p202 a、p202 b和p204调节多种细胞因子的活性。 转录因子，也参与肌肉分化。PKR是一种多功能的丝氨酸/苏氨酸激酶，参与抗病毒防御和细胞生长控制，并参与应答 各种压力信号。我们之前报道过，在培养的C2 C12成肌细胞分化为肌管的过程中，由于骨骼肌特异性转录因子的反式激活，p204的水平增加。 MyoD蛋白。p202 a、p202 b和PKR的水平在分化过程中也增加。我们在这里报告说，这些增加的蛋白质水平也是由于MyoD对其基因的反式激活。 这是由于在这些基因中的每一个中存在至少六个E盒，这是MyoD的识别位点。我们还发现，p204，p202 a，p202 b和PKR蛋白的分布， 在野生型小鼠和缺乏IFN-α、IFN-β和IFN-γ受体的小鼠中，成年C129小鼠的五种组织中的表达相同。这表明合成和分布 未感染成年小鼠中这些蛋白质的含量不受内源性干扰素的影响。
The murine 200 family proteins p202a, p202b, and p204, and also RNA-dependent protein kinase (PKR) are inducible by interferons (IFNs). p202a, p202b, and p204 modulate the activity of a large variety of transcription factors and also are involved in muscle differentiation. PKR is a multifunctional serine/threonine kinase, which is involved in antiviral defense and cell growth control and in the response to various stress signals. We reported earlier that the level of p204 increases during cultured C2C12 myoblast differentiation to myotubes in consequence of transactivation by the skeletal muscle-specific MyoD protein. The levels of p202a, p202b, and PKR also increase during the differentiation. We report here that these increased protein levels also are due to the transactivation of their genes by MyoD. This is made possible by the occurrence in each of these genes of at least six E boxes, which are recognition sites for MyoD. We also show that the distribution of the p204, p202a, p202b, and PKR proteins in five tissues of adult C129 mice is the same in wild-type mice and mice lacking the IFN-α, IFN-β, and IFN-γreceptors. This indicates that the synthesis and distribution of these proteins in uninfected adult mice are not affected by endogenous IFNs.