PATHWAYS REGULATING AMOEBIC CYST FORMATION

调节阿米巴包囊形成的途径

• 批准号: 6127297
• 负责人: DANIEL J EICHINGER
• 金额: $ 37.13万
• 依托单位: NEW YORK UNIVERSITY SCHOOL OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-03-01 至 2004-02-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6127297
• 关键词: Entamoeba histolytica; N acetylglucosamine; amebiasis; antibody; binding proteins; binding sites; cell aggregation; cell differentiation; cell growth regulation; cell membrane; electron microscopy; enzyme linked immunosorbent assay; galactose; gene expression; genetic transcription; glycolipids; glycoproteins; immunofluorescence technique; lectin; life cycle; mucins; protein structure function; protozoal cyst; ubiquitin; western blottings

DESCRIPTION: (Adapted from the Applicant'ps Abstract): Encystation in the human parasite Entamoeba histolytica cannot be studied in vitro. The related reptilian parasite, E. invadens, will encyst in vitro and can be used as model system to study encystation in Entamoeba. Two sugars inhibit the amebic encystation process. Galactose prevents the aggregation of ameba, which precedes encystation while N acetyl glucosamine allows aggregation to occur but still prevents the formation of osmotically resistant cysts. This proposal will study the role of galactose ligands and their receptor in the encystment process. An ortholog of the light subunit of the GalNAc lectin of E. histolytica has been cloned from E. invadens. The E. invadens gene product binds galactose and mucin, appears to be found on the surface of the ameba and likely mediates the initial cellular aggregation step. Gal-terminated glycoconjugates stimulate encystation in a concentration-dependent manner and suggest a role for the lectin in parasite differentiation. The structure of the lectin and a proposed mechanism of regulating encystation will be examined in this proposal.

描述：(改编自申请者的PS摘要)：人体内的加密 寄生虫溶组织内阿米巴不能在体外进行研究。相关的 爬行动物寄生虫--入侵棘球绦虫在体外会被包囊，可以作为模型。 研究内阿米巴包囊的系统。两种糖抑制阿米巴 包埋过程。半乳糖可防止阿米巴聚集，而阿米巴 在N-乙酰氨基葡萄糖允许聚集的情况下 仍然可以防止形成抗渗透的包囊。这项提议将 半乳糖配体及其受体在包囊中的作用研究 进程。报道了E. 从入侵的E.inadens中克隆了溶组织蛋白。侵袭性肠杆菌基因产物 结合半乳糖和粘蛋白，似乎发现在阿米巴表面和 可能参与了最初的细胞聚集步骤。GAL-终止 糖偶联物以浓度依赖的方式刺激囊化，并 提示凝集素在寄生虫分化中的作用。的结构。 凝集素和一种拟议的调节囊化的机制将在 这项提议。