Shen-Li H, O'Hagan R C, Hou H, Horner J W, Lee H W, DePinho R A
Department of Microbiology and Immunology, Albert Einstein College of Medicine, New York, New York 10461 USA.
Genes Dev. 2000 Jan 1;14(1):17-22.
Loss of Max function in the mouse resulted in generalized developmental arrest of both embryonic and extraembryonic tissues at early postimplantation (approximately E5.5-6.5), coincident with loss or dilution of maternal Max stores in the expanding embryo in vivo and in blastocyst outgrowths in vitro. Developmentally arrested embryos were reduced in size and exhibited widespread cytological degeneration and feeble BrdU incorporation. Max and, by extension, the Myc superfamily, serve essential roles in early mammalian development and a maternal reservoir of Max exists in sufficient amount to sustain Myc superfamily function through preimplantation stages of development.
小鼠中Max功能的丧失导致植入后早期（约E5.5 - 6.5）胚胎和胚外组织普遍发育停滞，这与体内正在发育的胚胎以及体外囊胚外植体中母体Max储备的丧失或稀释同时发生。发育停滞的胚胎体积减小，表现出广泛的细胞退化和微弱的BrdU掺入。Max以及由此延伸的Myc超家族在早期哺乳动物发育中发挥着重要作用，并且母体Max储备量足以在发育的植入前阶段维持Myc超家族的功能。
