RETINOBLASTOMA GENE IN INFLAMMATION AND CANCER

炎症和癌症中的视网膜母细胞瘤基因

• 批准号: 7610471
• 负责人: Lorne J Hofseth
• 金额: $ 12.09万
• 依托单位: UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-08-01 至 2008-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7610471
• 关键词: Colitis; Computer Retrieval of Information on Scientific Projects Database; Cultured Cells; Funding; Grant; Inflammation; Inflammatory; Institution; Malignant Neoplasms; Mediating; Nitric Oxide; Physiological; Process; Research; Research Personnel; Resources; Retinoblastoma Genes; Retinoblastoma Protein; Role; Signal Pathway; Site; Source; United States National Institutes of Health; carcinogenesis; in vivo; insight; mouse model; polypeptide; tumorigenesis

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. This project proposes to examine the signaling pathways that drive inflammation-mediated carcinogenesis. It has been shown that hyperphosphorylation and inactivation of the retinoblastoma protein (pRb) is associated with nitric oxide-induced inflammation and tumorigenesis. The functional significance of this process will be examined in cultured cells. Furthermore, the sites of hyperphosphorylation on the pRb polypeptide will be determined, and the physiological role of pRb hyperphosphorylation on the colitis-to-cancer sequence will be assessed in mouse models in vivo. Dr. Hofseths studies will generate important mechanistic insights into how pro-inflammatory factors, such as nitric oxide, promote tumorigenesis.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 该项目旨在研究驱动炎症介导的致癌作用的信号通路。 研究表明，视网膜母细胞瘤蛋白（pRb）的过度磷酸化和失活与一氧化氮诱导的炎症和肿瘤发生有关。 这一过程的功能意义将在培养的细胞中进行检查。 此外，将确定pRb多肽上的过度磷酸化位点，并将在小鼠体内模型中评估pRb过度磷酸化对结肠炎-癌症序列的生理作用。 霍夫赛斯博士的研究将产生重要的机制的见解如何促炎因子，如一氧化氮，促进肿瘤发生。