ROLE OF ANKYRIN COMPLEXES IN ANOIKIS

锚蛋白复合物在失巢凋亡中的作用

• 批准号: 8167961
• 负责人: Steven Miles Frisch
• 金额: $ 21.91万
• 依托单位: WEST VIRGINIA UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-07-01 至 2011-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8167961
• 关键词: Actins; Address; Ankyrins; Anoikis; Apoptosis; Cells; Cellular biology; Complex; Computer Retrieval of Information on Scientific Projects Database; Cytoskeletal Proteins; Cytoskeleton; E-Cadherin; Epithelial Cells; Extracellular Matrix; Funding; Gene Expression; Grant; Institution; Journals; Laboratories; Link; Malignant Epithelial Cell; Oncogenic; Paper; Reporting; Research; Research Personnel; Resistance; Resources; Role; Source; United States National Institutes of Health; adhesion receptor; epithelial to mesenchymal transition; programs; response

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. Anoikis is defined as apoptosis that is inhibited by extracellular matrix; it was discovered by our laboratory and reported in a 1994 Journal of Cell Biology paper. We are focusing on the mechanisms by which the oncogenic EMT (epithelial-to-mesenchymal transition) confers resistance to anoikis upon carcinoma cells. In particular, we are investigating the role of ankyrins, cytoskeletal proteins that link the actin cytoskeleton to various transmembrane adhesion receptors including E-cadherin. We hypothesize that ankyrin expression in normal epithelial cells sets up a transcriptional program that permits cells to die in response to cell-matrix detachment. Conversely, we posit that the loss of ankyrin that occurs frequently in carcinoma cells establishes an anoikis-resistance gene expression program. This project addresses these hypotheses

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。 失巢凋亡被定义为细胞外基质抑制的细胞凋亡;它是由我们的实验室发现的，并在1994年的细胞生物学杂志论文中报道。 我们的重点是致癌EMT（上皮细胞间质转化）赋予癌细胞抗失巢凋亡的机制。特别是，我们正在研究锚蛋白的作用，细胞骨架蛋白连接肌动蛋白细胞骨架的各种跨膜粘附受体，包括E-钙粘蛋白。 我们假设锚蛋白在正常上皮细胞中的表达建立了一个转录程序，允许细胞在细胞-基质脱离时死亡。 相反，我们认为锚蛋白的丢失在癌细胞中频繁发生，建立了一个抗失巢凋亡基因表达程序。 本项目解决这些假设