COBRE: USC: RETINOBLASTOMA GENE IN INFLAMMATION AND CANCER

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。我们在这个实验室有三个主要项目。第一个项目是通过刚刚从NIH收到的一笔校外赠款资助的（R21，直接费用275，000美元，开始日期：2006年1月4日），涉及检查人参和银杏对结肠炎和癌症中一氧化氮途径的影响。这是与Mike Wargovich博士合作的。到目前为止，我们已经表明人参抑制一氧化氮的产生，这可能会导致结肠癌的抑制，因为一氧化氮已被证明是这种疾病的驱动力。 第二个项目（R 01待定）涉及与结肠炎相关的结肠癌中pRb途径的检查（Ying等人，Cancer Research，2005）。该项目继续发展，我们已经表明，一氧化氮是结肠炎中pRb通路失调的关键介质，并可能提供结肠癌的机制。我们的计划是在未来6个月内向高影响力的期刊提交一篇论文。最后，与Mike Wyatt博士合作，我们正在研究碱基切除修复（BER）途径，慢性炎症和一氧化氮。BER途径中的特定糖基化酶（AAG）具有控制AAG功能的酪氨酸。一氧化氮物质通过硝化酪氨酸残基并改变靶蛋白的功能来靶向酪氨酸残基。这表明，AAG是一氧化氮的目标，这发生在慢性炎症和肿瘤发生。今后的工作旨在继续收集所有待审研究和资助研究的数据。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. We have three main projects in this lab. The first, funded through an extramural grant just received from the NIH (R21, $275,000 direct costs, start date: 04/01/2006) involves examining the effects of Ginseng and Ginkgo on the nitric oxide pathway in colitis and cancer. This is in collaboration with Dr. Mike Wargovich. We have so far shown that Ginseng inhibits nitric oxide production, which may lead to an inhibition of colon cancer since nitric oxide has been shown to drive this disease. The second project (R01 pending) involves the examination of the pRb pathway in colon cancer associated with colitis (Ying et al., Cancer Research, 2005). This project continues to evolve, and we have shown that nitric oxide is a key mediator of pRb pathway dysregulation in colitis, and may provide a mechanism toward colon cancer. Our plan is to submit a paper to a high impact journal in the next 6 months. Finally, in collaboration with Dr. Mike Wyatt, we are examining the base excision repair (BER) pathway, chronic inflammation, and nitric oxide. A specific glycosylase in the BER pathway (AAG) has a tyrosine that controls AAG function. Nitric oxide species target tyrosine residues by nitrating them, and changing the function of the targeted protein. It is suggested that AAG is a target of nitric oxide and that this occurs in chronic inflammation and tumorigenesis. Future work is aimed at continuing collection of data for all pending and funded studies.