ANION TRANSPORT IN EHRLICH CARCINOMA CELLS
埃利希癌细胞中的阴离子转运
基本信息
- 批准号:3170798
- 负责人:
- 金额:$ 4.44万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1982
- 资助国家:美国
- 起止时间:1982-07-01 至 1988-06-30
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
The overall objective of our research is the characterization of the
inorganic anion permeability pathways of the Ehrlich mouse ascites
carcinoma cell. The kinetic characteristics of chloride, sulfate, and
inorganic phosphate transport across the plasma membrane suggest that in
order for these anions to enter the cell they must first interact with
specific membrane carrier systems. Previous studies have provided evidence
consistent with the view that chloride and sulfate utilize a single carrier
system possessing two reactive sites, while phosphate utilizes an entirely
separate system. Recent studies have shown that chloride utilizes three
separate permeability pathways: nonmediated diffusion (10%), co-transport
with potassium and sodium (40%), and mediated self-exchange through the
anion transporter (50%). During the past year, we have investigated the
co-transport pathway in some detail. Our results show that in order for
chloride to be transported by this mechanism both potassium and sodium are
required.
In cells under steady state (physiological) conditions, the anion/cation
stoichiometry at 37~C is: 2Cl:1Na:1K. Chloride transport mediated by the
anion exchanger (Cl self-exchange) exhibits self-inhibition at high
extracellular chloride which is abolished when pHo is lowered to 5.5. This
finding suggests that H+ interacts at a modifier (inhibitory) site on the
anion transporter and in so doing relieves inhibition. In contrast to
chloride, about 85% of phosphate transport depends on the presence of
sodium in the extracellular medium. We have shown that monovalent
phosphate is the predominate, if not exclusive, species transported and
that a decrease in intracellular pH results in inhibition of transport. In
the next year of this project, we plan to further characterize the cation
requirements of the chloride-cation co-transport pathway. We are
particularly interested in the mechanism by which this transport system
switches from a bi-directional exchange during the physiological steady
state (constant cell volume) to a net transport pathway when the tumor cell
volume regulates. (A)
我们研究的总体目标是表征
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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CHARLES LEVINSON其他文献
CHARLES LEVINSON的其他文献
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{{ truncateString('CHARLES LEVINSON', 18)}}的其他基金
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