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首页> 外文期刊>Molecular and Cellular Biology >The nerve growth factor-responsive PC12 cell line does not express the Myc dimerization partner Max.
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The nerve growth factor-responsive PC12 cell line does not express the Myc dimerization partner Max.

机译：神经生长因子反应性PC12细胞系不表达Myc二聚体伴侣Max。

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摘要

Heterodimerization of Max with the nuclear oncoprotein Myc and the differentiation-associated proteins Mad and Mxi1 enables these factors to bind E-box sites in DNA and control genes implicated in cell proliferation and differentiation. We show that in the PC12 pheochromocytoma tumor cell line, functional Max protein is not expressed because of the synthesis of a mutant max transcript. This transcript encodes a protein incapable of homo- or heterodimerization. Furthermore, the mutant Max protein, unlike wild-type Max, is incapable of repressing transcription from an E-box element. Synthesis of mutant max transcripts appears to be due to a homozygous chromosomal alteration within the max gene. Reintroduction of max into PC12 cells results in repression of E-box-dependent transcription and a reduction in growth rate, which may explain the loss of Max expression either during the growth of the pheochromocytoma or in subsequent passage of the PC12 cell line in vitro. Finally, the ability of these cells to divide, differentiate, and apoptose in the absence of Max demonstrates for the first time that these processes can occur via Max- and possibly Myc-independent mechanisms.
机译：Max与核癌蛋白Myc以及分化相关蛋白Mad和Mxi1的异源二聚化作用使这些因子能够结合DNA中的E-box位点并控制与细胞增殖和分化有关的基因。我们显示，在PC12嗜铬细胞瘤肿瘤细胞系中，由于合成了一个突变的最大转录本，未表达功能性Max蛋白。该转录物编码不能同源二聚或异源二聚化的蛋白质。此外，与野生型Max不同，突变型Max蛋白不能抑制E-box元件的转录。突变体最大转录物的合成似乎是由于最大基因内的纯合染色体改变。将max重新引入PC12细胞会导致E-box依赖的转录受到抑制并降低生长速率，这可能解释了嗜铬细胞瘤生长过程中或随后PC12细胞系在体外传代过程中Max表达的丧失。最后，在没有Max的情况下，这些细胞分裂，分化和凋亡的能力首次证明了这些过程可以通过Max或可能独立于Myc的机制发生。

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