The Center for the Biology of Chronic Disease (CBCD), 616 Corporate Way, Suite 2-3665, Valley Cottage, New York City, NY 10989 USA.
Cell Mol Biol Lett. 2018 Nov 26;23:56. doi: 10.1186/s11658-018-0121-1. eCollection 2018.
CBP and p300 are histone acetyltransferase coactivators that control the transcription of numerous genes in humans, viruses, and other organisms. Although two separate genes encode CBP and p300, they share a 61% sequence identity, and they are often mentioned together as p300/CBP. Zhou et al. showed that under hypoxic conditions, HIF1α and the tumor suppressor p53 compete for binding to the limiting p300/CBP coactivator. Jethanandani & Kramer showed that δEF1 and MYOD genes compete for the limited amount of p300/CBP in the cell. Bhattacharyya et al. showed that the limiting availability of p300/CBP in the cell serves as a checkpoint for HIF1α activity. Here, we use the microcompetition model to explain how latent viruses with a specific viral cis-regulatory element in their promoter/enhancer can disrupt this competition, causing diseases such as cancer, diabetes, atherosclerosis, and obesity.
CBP 和 p300 是组蛋白乙酰转移酶共激活因子,可控制人类、病毒和其他生物体中许多基因的转录。尽管有两个独立的基因编码 CBP 和 p300,但它们具有 61%的序列同一性,并且通常一起被提及为 p300/CBP。Zhou 等人表明,在缺氧条件下,HIF1α 和肿瘤抑制因子 p53 竞争结合有限的 p300/CBP 共激活因子。Jethanandani 和 Kramer 表明,δEF1 和 MYOD 基因竞争细胞中有限数量的 p300/CBP。Bhattacharyya 等人表明,细胞中 p300/CBP 的有限可用性可作为 HIF1α 活性的检查点。在这里,我们使用微竞争模型来解释具有特定病毒顺式调控元件的潜伏病毒如何破坏这种竞争,从而导致癌症、糖尿病、动脉粥样硬化和肥胖等疾病。