Induced recovery of defective membrane expression of a CC chemokine receptor 5 mutant by phytohemagglutinin |
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Authors: | Q.-Y.?Qi,F.?Wang,H.-T.?Zhang,J.-C.?Wang,H.-P.?Xiao,M.-H.?Wang,Y.-F.?Han,R.-M.?Zhang,S.-H.?Tao,Z.?W.?Luo mailto:z.luo@bham.ac.uk" title=" z.luo@bham.ac.uk" itemprop=" email" data-track=" click" data-track-action=" Email author" data-track-label=" " >Email author |
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Affiliation: | (1) Laboratory of Population & Quantitative Genetics, The State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Morgan-Tan International Center for Life Sciences (MTIC), Fudan University, 200433 Shanghai, 220 Handan Road, China;(2) Department of Tuberculosis, Shanghai Pulmonary Hospital, 200433 Shanghai, 507 Zhengmin Road, China;(3) School of Biosciences, University of Birmingham, Birmingham, United Kingdom |
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Abstract: | ![]() CC chemokine receptor 5 (CCR5) is a member of the G-protein-coupled receptor superfamily. It plays an important role in macrophage tropic human immunodeficiency virus-1 entry and in some inflammatory reactions. CCR5-893(–) is a single-nucleotide deletion that results in complete truncation of the C tail of the gene product. We detected CCR5-893(–) in a sample of patients infected with non-tuberculosis mycobacteria and found that it was maintained heterozygously with a frequency of 2%. There is no association between this mutation and any immunodeficiency. Membrane expression of CCR5-893(–) was substantially reduced compared to the wild type, but this defective surface presentation recovered greatly recovered in the presence of 2 mg l-1 phytohemagglutinin (PHA). However, PHA inducement did not affect the total intracellular expression of CCR5-893(–) or wild-type CCR5. Thus we suggest there exist some PHA-induced factor(s) that could mediate the presentation of truncated CCR5.Received 23 July 2003; accepted 18 August 2003 |
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Keywords: | CCR5-893(– ) immunodeficiency membrane expression PHA inducement |
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