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全基因组p63-目标基因分析揭示了TAP63/NRF2-依赖氧化应激反应

Marco Napoli^1,2, Avani A Deshpande^1,2, Deepavali Chakravarti³

¹Department of Molecular Oncology, Division of Basic Science, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.

Cancer research communications

|January 2, 2024

概括

通过与不同的转录因子相互作用,p63异型TAp63和ΔNp63控制皮肤细胞功能. 这导致了独特的基因表达程序,解释了它们在发育和疾病中的多样性作用.

科学领域:

分子生物学分子生物学
发展生物学发展生物学
癌症生物学癌症生物学

背景情况:

TP63基因编码TAp63和ΔNp63异型,它们在表皮发育和癌症中发挥着不同的作用.
尽管共享DNA结合域,但这些异构体调节独特的生物功能,包括干细胞的维护,分化和衰老.
了解这些独特功能背后的分子机制对于理解上皮细胞生物学和疾病至关重要.

研究的目的:

阐明由 TAp63 和 ΔNp63 异型调节的独特的转录程序.
鉴定这些异构体尽管结构相似,但实现功能多样性的机制.
在表皮细胞中发现由p63异型控制的新型相互作用和通路.

主要方法:

包括p63异型特异性染色体免疫沉 (ChIP) 在内的全基因组分析.
RNA测序 (RNA-seq) 用于分析基因表达变化.
代谢学:用于评估小鼠TAp63-/-和ΔNp63-/-表皮细胞中的代谢变化.

主要成果:

TAp63和ΔNp63与不同的转录因子相互作用,调节独特的下游目标基因.
识别由每种p63异型特异控制的新型转录组.
在调节新陈代谢途径和氧化应激反应方面,TAp63和NRF2之间已经证明了合作.

结论:

通过与不同转录因子的相互作用,p63异型通过与不同转录因子的相互作用实现功能特异性,从而产生不同的转录输出.
这些发现提供了对p63在表皮平衡,衰老和潜在的癌症中的多样性作用的机制性见解.
这项研究强调了异形特异性调节在复杂的生物过程中的重要性.

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