INTEGRIN ASSOCIATED PROTEINS

整合素相关蛋白

• 批准号: 7957753
• 负责人: Kenneth Yamada
• 金额: $ 0.33万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-09-01 至 2010-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7957753
• 关键词: Actins; Adhesions; Biology; Cell Proliferation; Cell physiology; Cell-Matrix Junction; Complex; Computer Retrieval of Information on Scientific Projects Database; Cytoskeleton; Extracellular Matrix; Funding; Fungal Genome; Future; Grant; Institution; Integrins; Ligands; Malignant Epithelial Cell; Malignant Neoplasms; Molecular; Mouth Carcinoma; Neoplasm Metastasis; Pathway interactions; Phenotype; Proteomics; Regulation; Research; Research Personnel; Resources; Signal Pathway; Source; United States National Institutes of Health; cell motility; extracellular; malignant mouth neoplasm; migration; receptor; receptor binding

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. Integrin receptors bind to extracellular matrix (ECM) ligands and selectively connect to intracellular signaling pathways and the actin cytoskeleton to regulate adhesion-dependent cellular processes. In cancer, the dynamic regulation of adhesion by integrins is critical for cell attachment to ECM, cell proliferation, invasion and cell migration. However, the intracellular downstream effectors of integrins that are important for oral cancer migration, invasion and metastasis are not well understood. Our aim is to compare the composition of integrin associated complexes derived from highly and poorly metastatic oral carcinoma cells. This proteomics study will identify candidate integrin downstream factors that either associate with distinct integrin receptors or specifically associate with integrins in a particular metastatic state. Future studies will delineate whether the identified factors regulate invasion and metastasis, as well as the molecular pathways involved in regulating these metastatic phenotypes.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 整联蛋白受体与细胞外基质（ECM）配体结合，并有选择地连接到细胞内信号通路和肌动蛋白细胞骨架，以调节依赖于粘附的细胞过程。在癌症中，整合素对粘附的动态调节对于细胞附着ECM，细胞增殖，侵袭和细胞迁移至关重要。但是，对口腔癌迁移，侵袭和转移至关重要的整联蛋白的细胞内下游效应子尚不清楚。我们的目的是比较源自高度和不良转移性口服癌细胞的整合素相关复合物的组成。这项蛋白质组学研究将确定候选整合素的下游因子，这些因素要么与独特的整合素受体相关，要么在特定转移性状态下与整合蛋白特别相关。未来的研究将描述确定的因素是否调节侵袭和转移，以及与调节这些转移表型有关的分子途径。