Hypoxia regulation of gene transcription
Hypoxia regulation of gene transcription
复制标题
DOI：
10.1089/152702901750265251
复制
发表时间：
2001-06-01
影响因子：
2.1
通讯作者：
Caro, J
中科院分区：
文献类型：
--
作者：
Caro, J
对缺氧的适应性反应包括各种基因的转录激活，如那些编码糖酵解酶、生长因子和血管活性肽的基因，这些基因往往会改善缺氧的损伤作用。这些基因中的大多数受缺氧诱导因子1复合物（HIF-1）的调节，HIF-1是一种异二聚体蛋白复合物，其通过与存在于这些基因中的特异性缺氧反应序列（HRE）结合来激活转录。低氧通过稳定HIF-1 α亚基诱导HIF-1复合物的形成，HIF-1 α亚基在常氧条件下被泛素-蛋白酶体系统降解。细胞感受缺氧信号和抑制缺氧反应的分子机制尚不清楚。更被接受的氧传感模型涉及血红素蛋白传感器的参与，或者基于可能涉及或不涉及线粒体参与的氧化还原反应。
The adaptive responses to hypoxia include the transcriptional activation of various genes like those encoding for glycolytic enzymes, growth factors and vasoactive peptides that tend to ameliorate the damaging effect of the lack of oxygen. Most of these genes are regulated by the hypoxia-inducible factor 1 complex (HIF-1), a heterodimer protein complex that activates transcription through binding to specific hypoxic-responsive sequences (HRE) present in those genes. Hypoxia induces HIF-1 complex formation by stabilizing the HIF-1 alpha sub-unit, which under normoxic conditions is degraded by the ubiquitin-proteasome system. The molecular mechanisms by which cells sense the hypoxic signal and transduce the hypoxic response are still not clear. The more accepted models for oxygen sensing involve the participation of heme-proteins sensors or are based in redox-reactions which may or not involve participation of mitochondria.