SIGNAL TRANDUCTION IN POLYCYTHEMIA VERA
真性红细胞增多症的信号转导
基本信息
- 批准号:6030835
- 负责人:
- 金额:$ 30.95万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1997
- 资助国家:美国
- 起止时间:1997-08-01 至 2000-06-30
- 项目状态:已结题
- 来源:
- 关键词:apoptosis biological signal transduction erythroid stem cell erythropoietin flow cytometry gene expression genetic regulation growth factor human subject megakaryocytes myeloid stem cell neutrophil phosphorylation platelets polycythemia vera polymerase chain reaction protein tyrosine kinase thrombopoietic factor tissue /cell culture tumor suppressor genes
项目摘要
DESCRIPTION: The long term objective of our research is to define the
mechanisms responsible for polycythemia vera (PV), a clonal disorder of
unknown etiology which involves erythroid, myeloid and megakaryocytic
progenitor cells. Recent studies in our laboratory have indicated that PV
erythroid progenitor cells, in contrast to normal erythroid progenitor
cells, are resistant to the apoptosis associated with erythropoietin (EPO)
deprivation. We have also identified a novel signal transduction defect in
PV platelets involving thrombopoietin (TPO)-mediated protein tyrosine
phosphorylation. These observations have important implications with
respect to both the pathogenesis of PV and its clinical manifestations.
Based on our observations to date, we now plan to examine TPO-mediated PV
platelet signal transduction with respect to platelet c-Mpl expression, the
interaction of c-Mpl in PV megakaryocytes as compared to PV platelets. To
identify the mechanisms for apoptosis-resistance in PV, using a liquid
suspension culture system capable of expanding the population of both normal
and PV peripheral blood erythroid progenitor cells, we plan to examine the
mechanisms involved in the expression and regulation of Bcl-2 family genes
and p53 in the presence and absence of EPO, and using neutrophils as a
surrogate model for myeloid cells, to determine whether the
apoptosis-resistance associated with growth factor deprivation and its
mechanism are global characteristics of PV hematopoiesis.
描述:我们研究的长期目标是定义
项目成果
期刊论文数量(2)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
A novel thrombopoietin signaling defect in polycythemia vera platelets.
真性红细胞增多症血小板中一种新型血小板生成素信号缺陷。
- DOI:10.1002/stem.5530160721
- 发表时间:1998
- 期刊:
- 影响因子:0
- 作者:Moliterno,AR;Siebel,KE;Sun,AY;Hankins,WD;Spivak,JL
- 通讯作者:Spivak,JL
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Jerry L Spivak其他文献
Jerry L Spivak的其他文献
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{{ truncateString('Jerry L Spivak', 18)}}的其他基金
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ROLE OF CELL ADHESION IN BIOLOGICAL SIGNAL TRANSDUCTION
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- 批准号:
6238317 - 财政年份:1997
- 资助金额:
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