Zhu H, Bunn H F
Division of Hematology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Respir Physiol. 1999 Apr 1;115(2):239-47. doi: 10.1016/s0034-5687(99)00024-9.
A growing number of physiologically relevant genes are regulated in response to changes in intracellular oxygen tension. It is likely that cells from a wide variety of tissues share a common mechanism of oxygen sensing and signal transduction leading to the activation of the transcription factor hypoxia-inducible factor 1 (HIF-1). Besides hypoxia, transition metals (Co2+, Ni2+ and Mn2+) and iron chelation also promote activation of HIF-1. Induction of HIF-1 by hypoxia is blocked by the heme ligands carbon monoxide and nitric oxide. There is growing, albeit indirect, evidence that the oxygen sensor is a flavoheme protein and that the signal transduction pathway involves changes in the level of intracellular reactive oxygen intermediates. The activation of HIF-1 by hypoxia depends upon signaling-dependent rescue of its alpha-subunit from oxygen-dependent degradation in the proteasome, allowing it to form a heterodimer with HIF-1beta (ARNT), which then translocates to the nucleus and impacts on the transcription of genes whose cis-acting elements contain cognate hypoxia response elements.
越来越多的生理相关基因会根据细胞内氧张力的变化而受到调控。来自多种组织的细胞可能共享一种氧感应和信号转导的共同机制,该机制会导致转录因子缺氧诱导因子1(HIF-1)的激活。除了缺氧,过渡金属(Co2+、Ni2+和Mn2+)以及铁螯合也会促进HIF-1的激活。缺氧诱导的HIF-1激活会被血红素配体一氧化碳和一氧化氮所阻断。越来越多的证据(尽管是间接的)表明,氧传感器是一种黄素血红素蛋白,并且信号转导途径涉及细胞内活性氧中间体水平的变化。缺氧对HIF-1的激活取决于信号依赖性地将其α亚基从蛋白酶体中依赖氧的降解中拯救出来,使其能够与HIF-1β(ARNT)形成异二聚体,然后该异二聚体转运至细胞核并影响那些顺式作用元件包含同源缺氧反应元件的基因的转录。