SEARCH FOR NOVEL B CELL HYPERACTIVITY GENES
寻找新型 B 细胞过度活跃基因
基本信息
- 批准号:6100391
- 负责人:
- 金额:$ 15.9万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1998
- 资助国家:美国
- 起止时间:1998-12-01 至 1999-11-30
- 项目状态:已结题
- 来源:
- 关键词:B lymphocyte CD5 molecule animal genetic material tag apoptosis biological signal transduction cell differentiation complementary DNA flow cytometry gene expression genetic strain immunogenetics laboratory mouse leukocyte activation /transformation messenger RNA molecular cloning northern blottings nucleic acid sequence polymerase chain reaction receptor expression systemic lupus erythematosus
项目摘要
Our long-term goal is to identify the genes and their products that
determine hyperactivity of B cells, particularly B-1 (DC5-lineage) B
cells. New Zealand Black (NZB) mice, that have a life-long
hyperactivity ob B-1 cells, will be studied. NZB mice not only
develop autoimmune disease but also a high incidence of malignant
lymphomas of B-1 B cells that are very similar to human CLL and the
B cell lymphomas developing the AIDS patients. In addition B-1 B
cells are hyperactive in the inflamed joints of rheumatoid arthritis (RA)
patients where they play a major role in antigen presentation and
activation of inflammatory cells. We have preliminary evidence
showing that the hyperactive B cells of NZB mice differentially express
several genes that are not expressed in normal B cells. In this
development and feasibility study, we would like to confirm the
identity of these B cell hyperactivity genes. Eventually we aim to
clone the full length cDNA for these differentially expressed genes,
sequence them, study their genomic organization and define their
function. This search for B cell hyperactivity genes may reveal novel
genes or new function for known genes. Besides its relevance to RA
and malignant B cell lymphomas as stated above, this project could
enhance our understanding of the basic mechanisms of B cell
differentiation, signal transduction, tolerance and apoptosis.
我们的长期目标是确定基因和它们的产物
项目成果
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{{ truncateString('SYAMAL K DATTA', 18)}}的其他基金
IMMUNE MECHANISMS OF ANTICD40L TRIAL IN SLE
SLE 中 ANTICD40L 试验的免疫机制
- 批准号:
2882256 - 财政年份:1999
- 资助金额:
$ 15.9万 - 项目类别:
IMMUNE MECHANISMS OF ANTICD40L TRIAL IN SLE
SLE 中 ANTICD40L 试验的免疫机制
- 批准号:
6137339 - 财政年份:1999
- 资助金额:
$ 15.9万 - 项目类别:
IMMUNE MECHANISMS OF ANTICD40L TRIAL IN SLE
SLE 中 ANTICD40L 试验的免疫机制
- 批准号:
6341792 - 财政年份:1999
- 资助金额:
$ 15.9万 - 项目类别:
相似海外基金
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CD5分子的生物学功能分析。
- 批准号:
63480170 - 财政年份:1988
- 资助金额:
$ 15.9万 - 项目类别:
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