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中文摘要
翻译
这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金, 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 本研究主要研究HIV-1在肺泡巨噬细胞中复制的转录调控。来自非炎症肺的肺泡巨噬细胞通过表达16 kDa抑制形式的转录因子C/EBPB(也称为NF-IL6和LIP)来抑制HIV-1的复制,从而在肺部产生潜在的HIV-I感染。对结核病的炎症反应减少了C/EBPB的表达,降低了HIV-1的长端重复序列,并诱导了C/EBP转录因子家族的另一个成员,该转录因子家族支持HIV-1在肺部的高水平复制。该实验室用于以下方面:DNA提取、DNA测序(自动化)、ELISA、寡核苷酸合成、聚合酶链式反应、重组DNA技术、RNA提取、Southern分析、Western分析、支气管肺泡灌洗液处理、EMSA和层流罩的使用。
英文摘要
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 study focuses on the transcriptional regulation of HIV-1 replication in alveolar macrophages. Alveolar macrophages from uninflamed lung inhibit HIV-1 replication by expressing a 16kDa inhibitory form of transcription factor C/EBPB (also called NF-IL6 and LIP) producing latent HIV-I infection in the lung. The inflammatory response to tuberculosis reduces C/EBPB expression, derepressing the HIV-1 long terminal repeat and induces another member of the C/EBP transcription factor family which supports high level HIV-1 replication in the lung. The lab was used for the following: DNA isolation, DNA sequencing (automated), ELISA, oligonucleotide synthesis, PCR, recombinant DNA techniques, RNA isolation, Southern analysis, Western analysis, bronchoalveolar lavage processing, EMSA, and use of laminar flow hoods.
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Treatment response of WTC related airway injury
Evolution of Risk Factors for Sinusitis in WTC Exposed Firefighters
HIV activation in secondary pulmonary infection
HIV activation in secondary pulmonary infection
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