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Chemokine receptor CCR5: polymorphism at protein level
Shunji Suzuki1, Tomoko Miyagi, Linda F Chuang
1Department of Medical Pharmacology and Toxicology, University of California, Davis, CA 95616, USA.
Biochemical and Biophysical Research Communications
|August 7, 2002
Summary
Two distinct chemokine receptor CCR5 (CC chemokine receptor type 5) protein forms, 62 kDa and 42 kDa, exist in human and monkey cells. Their expression is modulated by cell growth, chemical agents, and HIV-related factors.
Area of Science:
- Immunology and Virology
- Molecular Cell Biology
Background:
- Chemokine receptor CCR5 (CC chemokine receptor type 5) gene polymorphisms are linked to HIV disease progression and resistance.
- Previous research identified diverse CCR5 transcripts and mRNA variants.
Purpose of the Study:
- To investigate the existence and characteristics of distinct CCR5 protein forms in human and monkey cells.
- To explore the regulation of these CCR5 forms by cell growth and specific chemical agents.
Main Methods:
- Western blot analysis to detect and differentiate CCR5 protein forms (62 kDa and 42 kDa) in cellular extracts.
- Cellular localization studies using techniques to determine the subcellular distribution of each CCR5 form.
- Treatment of cells with morphine sulfate, RANTES, MIP-1alpha, and MIP-1beta to assess their effects on CCR5 expression.
Main Results:
- Two distinct CCR5 protein forms (62 kDa and 42 kDa) were identified in human lymphocytic and monkey peripheral blood mononuclear cells.
- The ratio of these two forms varied with cell growth, and they were not interconvertible.
- Morphine sulfate induced both CCR5 forms, while RANTES, MIP-1alpha, and MIP-1beta inhibited their expression.
- The 62 kDa CCR5 was primarily located on the cell membrane, and the 42 kDa CCR5 was found in the cytoplasm.
Conclusions:
- Evidence supports the presence of at least two distinct CCR5 protein isoforms with differential cellular localization.
- The expression and distribution of these CCR5 forms are dynamically regulated by cellular conditions and external stimuli, potentially impacting HIV infection dynamics.