FUNCTIONS OF APOLIPOPROTEINS IN CANCER APOPTOSIS

载脂蛋白在癌症细胞凋亡中的功能

• 批准号: 7960232
• 负责人: Chien-An Andy Hu
• 金额: $ 9.65万
• 依托单位: NEW MEXICO STATE UNIVERSITY LAS CRUCES
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-05-01 至 2010-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7960232
• 关键词: Amino Acids; Apolipoproteins; Apoptosis; Autophagocytosis; Biological Markers; Biomedical Research; Cell Death; Cells; Computer Retrieval of Information on Scientific Projects Database; DNA; Diagnosis; Eating; Fatty Acids; Funding; Grant; Human; Institution; Lipids; Malignant Neoplasms; Molecular; New Mexico; Nucleic Acids; Proteins; RNA; Recycling; Research; Research Personnel; Resources; Source; United States National Institutes of Health; cancer cell; cell injury; cell type; macromolecule; outcome forecast

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 continue investigating functions of apolipoprotein L1 (ApoL1) and ApoL2 in the induction of autophagy, a self-eating mechanism, in cancer cell death. Autophagy is normally used by cells to recycle the building blocks, such as amino acids, nucleic acids and fatty acids, for resynthesize macromolecules, such as proteins, DNA and RNA and lipids. Recent study also showed that autophagy can function as a programmed cell death mechanism to eliminate damaged cells. Our recent results showed that ApoL1 is one of the molecular regulators that induces autophagic cell death in various cancer cell types and its closely related protein ApoL2 can synergistically enhance ApoL1-induced cell death. Both ApoL1 and L2 are potential biomarkers for diagnosis, prognosis and treatment of human cancers.

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表示。列出的机构是 对于中心，这不一定是调查员的机构。 我们继续研究癌细胞死亡中载脂蛋白L1（Apol1）和Apol2的载脂蛋白L1（Apol1）和Apol2的功能。自噬通常被细胞用于回收构建块，例如氨基酸，核酸和脂肪酸，以重新合成大分子，例如蛋白质，DNA和RNA和脂质。最近的研究还表明，自噬可以用作消除受损细胞的程序性细胞死亡机制。我们最近的结果表明，APOL1是在各种癌细胞类型中诱导自噬细胞死亡的分子调节剂之一，其密切相关的蛋白质APOL2可以协同增强APOL1诱导的细胞死亡。 APOL1和L2都是人类癌症诊断，预后和治疗的潜在生物标志物。