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题目:: Transcription profiling of human and mouse keratinocytes infected with AD and Ad-NotchIC viruses reveals cross-regulation between Notch and p63 in keratinocyte commitment to differentiation
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状态:: 发布时间June 13, 2008 , 更新时间 March 27, 2012 , 提交时间 July 5, 2006,
物种:: Homo sapiens, Mus musculus
摘要:: Notch signaling promotes commitment of keratinocytes to differentiation and suppresses tumorigenesis. p63, a p53 family member, has been implicated in establishment of the keratinocyte cell fate and/or maintenance of epithelial self-renewal. Here we show that p63 expression is suppressed by Notch1 activation in both mouse and human keratinocytes through a mechanism independent of cell cycle withdrawal and requiring down-modulation of selected interferon-responsive genes, including IRF7 and/or IRF3. In turn, elevated p63 expression counteracts the ability of Notch1 to restrict growth and promote differentiation. p63 functions as a selective modulator of Notch1-dependent transcription and function, with the Hes-1 gene as one of its direct negative targets. Thus, a complex cross-talk between Notch and p63 is involved in the balance between keratinocyte self-renewal and differentiation. Experiment Overall Design: PolyA+ mRNA (2-5 ug) from cells infected with the Ad GFP and Ad-NotchIC viruses was used as template for double stranded cDNA preparations with a T7-(dT)24 oligonucleotide primers for the first strand reaction. The resulting cDNA was used for preparation of biotin-labeled antisense cRNA and further used for hybridization to Affymetrix U74A or U95A “gene chips” according to the manufacturer’s recommendation.
实验种类:: transcription profiling by array
样本量:: 4
实验设计:
: 无设计数据
数据号:: E-GEOD-5229, GSE5229
数据状态:: 无法自动分析，您可以尝试手动分析数据。

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