Id2 is dispensable for Myc-induced epidermal neoplasia.
Id2 is dispensable for Myc-induced epidermal neoplasia.
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Id2 对于 Myc 诱导的表皮瘤形成是可有可无的。
DOI：
10.1128/mcb.24.5.2083-2090.2004
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发表时间：
2004
影响因子：
5.3
通讯作者：
Evan,GerardI
中科院分区：
文献类型：
--
作者：
Murphy,DanielJ;Swigart,LamornaBrown;Israel,MarkA;Evan,GerardI
我们先前已经描述了一种表皮瘤形成的转基因小鼠模型，其中c-Myc的可转换形式MycERTAM的表达通过外皮蛋白启动子靶向于小鼠表皮的有丝分裂后基底上角质形成细胞。c-MycERTAM的持续激活导致进行性肿瘤表型，其特征在于基底上角质形成细胞的异常异位增殖和延迟分化，最终导致乳头状瘤病。Id 2基因的转录受Myc家族蛋白的调控。此外，Id 2被认为是多个谱系中细胞命运的关键决定因素，并通过其与视网膜母细胞瘤蛋白的相互作用在体外介导Myc依赖性细胞增殖中发挥作用。使用Id 2缺失小鼠，我们在体内评估了Id 2介导Myc诱导的皮肤乳头状瘤形成的需要。我们发现，Id 2的缺乏对Myc功能的任何可测量属性或最终肿瘤形成的时间或程度没有明显的影响。因此，我们的数据反对Id 2在体内介导Myc作用中的任何重要作用。
We have previously described a transgenic mouse model of epidermal neoplasia wherein expression of a switchable form of c-Myc, MycERTAM, is targeted to the postmitotic suprabasal keratinocytes of murine epidermis via the involucrin promoter. Sustained activation of c-MycERTAMresults in a progressive neoplastic phenotype characterized by aberrant ectopic proliferation and delayed differentiation of suprabasal keratinocytes, culminating in papillomatosis. Transcription of theId2gene is regulated by Myc family proteins. Moreover, Id2 is implicated as a pivotal determinant of cell fate in multiple lineages and has a demonstrated role in mediating Myc-dependent cell proliferation in vitro through its interaction with retinoblastoma protein. UsingId2nullizygous mice, we assessed in vivo the requirement for Id2 in mediating Myc-induced papilloma formation in skin. We show that absence of Id2 has no discernible impact on any measurable attribute of Myc function or on the timing or extent of eventual tumor formation. Thus, our data argue against any essential role for Id2 in mediating Myc action in vivo.