Ubiquitination, Intestinal Homeostasis and Cancer

摘要 成人肠道组织保持正常的功能状态，尽管快速增殖和 分化肠上皮细胞群，每隔6-7天补充上皮层。肠道 上皮细胞与肠道的适应性免疫细胞和先天免疫细胞密切相关。互惠 这些成分之间的动态对话维持肠道内环境的稳定，并部分地通过 旁分泌细胞因子和白介素网。肠炎易患肠上皮细胞(IEC) 通过不完全了解的机制向恶性转化。我们已经产生了一种新的撞车事件 自发性发育受扰的小鼠IEC分化，肠道伸长，并有高 对结肠癌的易感性。这些老鼠为我们提供了一个独特的机会来发现钥匙 调节肠道内环境平衡和推动IEC转化的炎性介质。vbl.使用 转录学、蛋白质组学、遗传上位论和细胞方法，我们的初步数据表明 在这些过程中的免疫细胞因子。

Abstract Adult intestinal tissues are maintained in a normal functional state despite rapidly proliferating and differentiating intestinal epithelial cell populations that replenish the epithelium layer every 6-7 days. Intestinal epithelial cells reside in close association with both adaptive and innate immune cells of the gut. A reciprocal and dynamic dialogue among these components maintains intestinal homeostasis and is mediated in part by paracrine cytokine and interleukin networks. Intestinal inflammation predisposes intestinal epithelial cells (IEC) to malignant transformation via incompletely understood mechanisms. We have generated a novel knock-in mouse line that spontaneously develops perturbed IEC differentiation, gut elongation, and have a high susceptibility to colon cancer. These mice provide us with a unique opportunity to discover the key inflammatory mediators that regulate intestinal homeostasis and drive IEC transformation. Using transcriptomic, proteomic, genetic epistasis and cellular approaches, our preliminary data implicate selected immune cytokines in these processes.