Ultraviolet A radiation-induced expression of human genes: molecular and photobiological mechanisms.
Ultraviolet A radiation-induced expression of human genes: molecular and photobiological mechanisms.
复制标题
紫外线 A 辐射诱导的人类基因表达：分子和光生物学机制。
作者：
Susanne Grether;R. Buettner;J. Krutmann
在暴露于紫外线（UV）辐射的哺乳动物细胞中，由于环境应激而增加的基因表达通常被观察到。在过去的几年里，对短波UVC （< 280nm）和中波UVB （280 - 320 nm）辐射诱导基因的顺式和反式遗传元件进行了很好的表征。最近，在了解长波UVA （320 - 400nm）辐射诱导人类基因转录激活的机制方面也取得了进展。从这些研究中，我们现在知道，UVA辐射诱导的基因表达的光生物学和分子机制与之前确定的UVB或uvc诱导的基因表达不同。特别是，活性氧单线态氧被发现是UVA辐射诱导的基因表达的主要效应物，通过诱导依赖于转录因子AP-2激活的信号转导级联。这些研究表明AP-2在哺乳动物应激反应中的作用以前未被认识到。
Increased gene expression as a consequence of environmental stress is typically observed in mammalian cells upon exposure to ultraviolet (UV) radiation. In previous years the cis- and trans-acting genetic elements responsible for gene induction by short wavelength UVC (< 280nm) and intermediate wavelength UVB (280 - 320 nm) radiation have been well characterized. More recently, progress has also been made in understanding the mechanisms by which long wavelength UVA (320 - 400 nm) radiation induces transcriptional activation of human genes. From these studies it is now known that the photobiological as well as the molecular mechanisms involved in UVA radiation-induced gene expression differ from those previously identified for UVB- or UVC-induced gene expression. In particular, the reactive oxygen species singlet oxygen was found to serve as the primary effector in UVA radiation-induced gene expression by inducing a signal transduction cascade that depends on activation of transcription factor AP-2. These studies indicate a previously unrecognized role of AP-2 in the mammalian stress response.