Myb-induced transformation.
Myb-induced transformation.
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DOI：
10.1615/critrevoncog.v7.i3-4.60
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发表时间：
1996
影响因子：
--
通讯作者：
Linda Wolff
中科院分区：
文献类型：
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作者：
Linda Wolff
c-myb原癌基因与禽类和鼠类骨髓和淋巴系造血系统肿瘤的发生有关。由该基因编码的转录因子在肿瘤发生中具有双重功能，因为它调节阻止细胞凋亡的基因和参与细胞增殖的基因。c-myb一再成为逆转录病毒插入诱变的靶。逆转录病毒激活c-myb的致癌潜力的最常见的机制是通过提供导致组成型表达的转录控制，这一特征与c-myb的异位表达可以防止分化的造血细胞的生长停滞的证明一致。在一种不太常见的激活机制中，羧基（C）末端截短使c-Myb蛋白在转录反式激活中更稳定和活跃。有趣的是，v-Myb，禽成髓细胞瘤病毒（AMV）的产物，在体内和体外引起细胞快速转化的能力，可以解释为通过逆转录病毒LTR，N-和C-末端截短，并激活其DNA结合结构域中的突变的表达失调的组合效应。虽然c-myb与人类白血病的关系已经被提出，但它从未被明确确定，应该进一步研究。
The c-myb protooncogene has been implicated in the development of avian and murine hematopoietic neoplasms of the myeloid and lymphoid lineages. The transcription factor encoded by this gene has a dual function in oncogenesis because it regulates genes that prevent apoptosis and genes involved in cellular proliferation. c-myb has repeatedly been a target of retroviral insertional mutagenesis. The most common mechanism by which retroviruses activate c-myb's oncogenic potential is by providing transcriptional control that results in constitutive expression, a feature that is consistent with the demonstration that ectopic expression of c-myb can prevent growth arrest of differentiating hematopoietic cells. In a less common mechanism of activation, carboxyl(C)-terminal truncation renders the c-Myb protein more stable and active in transcriptional transactivation. Interestingly, the ability of v-Myb, a product of the avian myeloblastosis virus (AMV), to cause rapid transformation of cells in vivo and in vitro can be explained by the combined effects of deregulated expression through the retroviral LTR, N- and C-terminal truncation, and activating mutations in its DNA binding domain. Although c-myb's involvement in human leukemia has been suggested, it has never been clearly established and should be investigated further.