Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, 50 South Drive, Bethesda, MD 20892, USA.
Sci Signal. 2010 Dec 14;3(152):pe49. doi: 10.1126/scisignal.3152pe49.
In the field of molecular oncology, the Myc basic helix-loop-helix family of transcription factors has been extensively studied. The Myc proto-oncogene c-Myc binds DNA, activates or represses gene transcription, and consequently affects cellular proliferation. However, emerging evidence presents the existence of c-Myc variants that lack transcriptional activity. A cytoplasmic variant of c-Myc called "Myc-nick," which arises from calpain-mediated cleavage of c-Myc, assists in stable microtubule assembly. Furthermore, Myc-nick promotes MyoD-mediated myogenic differentiation, thus antagonizing its precursor. These results provide exciting new opportunities in formulating molecular approaches for treatment of cancer and in our understanding of cell differentiation.
在分子肿瘤学领域，Myc 基本螺旋-环-螺旋家族转录因子已得到广泛研究。Myc 原癌基因 c-Myc 与 DNA 结合，激活或抑制基因转录，从而影响细胞增殖。然而，新出现的证据表明存在缺乏转录活性的 c-Myc 变体。c-Myc 的一种细胞质变体称为“Myc-nick”，它来源于钙蛋白酶介导的 c-Myc 切割，有助于稳定微管组装。此外，Myc-nick 促进 MyoD 介导的成肌分化，从而拮抗其前体。这些结果为制定治疗癌症的分子方法以及我们对细胞分化的理解提供了令人兴奋的新机会。
