Freytag S O, Geddes T J
Molecular Biology Research Program, Henry Ford Hospital, Detroit, MI 48202.
Science. 1992 Apr 17;256(5055):379-82. doi: 10.1126/science.256.5055.379.
3T3-L1 adipoblasts that express large amounts of c-Myc cannot terminally differentiate, raising the possibility that Myc inhibits the expression of genes that promote adipogenesis. The CCAAT/enhancer binding protein (C/EBP alpha) is induced during 3T3-L1 adipogenesis when cells commit to the differentiation pathway. Transfection of 3T3-L1 adipoblasts with the gene that encodes C/EBP alpha caused overt expression of the adipocyte morphology. Expression of Myc prohibited the normal induction of C/EBP alpha and prevented adipogenesis. Enforced expression of C/EBP alpha overcame the Myc-induced block to differentiation. These results provide a molecular basis for the regulation of adipogenesis and implicate Myc and C/EBP alpha as pivotal controlling elements.
大量表达c-Myc的3T3-L1脂肪前体细胞无法终末分化，这增加了Myc抑制促进脂肪生成的基因表达的可能性。在3T3-L1脂肪生成过程中，当细胞进入分化途径时，CCAAT/增强子结合蛋白（C/EBPα）会被诱导表达。用编码C/EBPα的基因转染3T3-L1脂肪前体细胞，会导致脂肪细胞形态的明显表达。Myc的表达阻止了C/EBPα的正常诱导并阻碍了脂肪生成。强制表达C/EBPα克服了Myc诱导的分化阻滞。这些结果为脂肪生成的调控提供了分子基础，并表明Myc和C/EBPα是关键的控制元件。
