putative cell surface receptor for anemia-inducing feline leukemia virus subgroup C is a member of a transporter superfamily

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Published inJournal of Virology Vol. 73; no. 8; pp. 6500 - 6505
Main Authors Tailor, C.S, Willett, B.J, Kabat, D
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.08.1999
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Online AccessGet full text
ISSN0022-538X
1098-5514
DOI10.1128/jvi.73.8.6500-6505.1999

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AbstractList Domestic cats infected with the horizontally transmitted feline leukemia virus subgroup A (FeLV-A) often produce mutants (termed FeLV-C) that bind to a distinct cell surface receptor and cause severe aplastic anemia in vivo and erythroblast destruction in bone marrow cultures. The major determinant for FeLV-C-induced anemia has been mapped to a small region of the surface envelope glycoprotein that is responsible for its receptor binding specificity. Thus, erythroblast destruction may directly or indirectly result from FeLV-C binding to its receptor. To address these issues, we functionally cloned a putative cell surface receptor for FeLV-C (FLVCR) by using a human T-lymphocyte cDNA library in a retroviral vector. Expression of the 2.0-kbp FLVCR cDNA in naturally resistant Swiss mouse fibroblasts and Chinese hamster ovary cells caused substantial susceptibility to FeLV-C but no change in susceptibilities to FeLV-B and other retroviruses. The predicted FLVCR protein contains 555 amino acids and 12 hydrophobic potential membrane-spanning sequences. Database searches indicated that FLVCR is a member of the major-facilitator superfamily of transporters and implied that it may transport an organic anion. RNA blot analyses showed that FLVCR mRNA is expressed in multiple hematopoietic lineages rather than specifically in erythroblasts. These results suggest that the targeted destruction of erythroblasts by FeLV-C may derive from their greater sensitivity to this virus rather than from a preferential susceptibility to infection.
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Domestic cats infected with the horizontally transmitted feline leukemia virus subgroup A (FeLV-A) often produce mutants (termed FeLV-C) that bind to a distinct cell surface receptor and cause severe aplastic anemia in vivo and erythroblast destruction in bone marrow cultures. The major determinant for FeLV-C-induced anemia has been mapped to a small region of the surface envelope glycoprotein that is responsible for its receptor binding specificity. Thus, erythroblast destruction may directly or indirectly result from FeLV-C binding to its receptor. To address these issues, we functionally cloned a putative cell surface receptor for FeLV-C (FLVCR) by using a human T-lymphocyte cDNA library in a retroviral vector. Expression of the 2.0-kbp FLVCR cDNA in naturally resistant Swiss mouse fibroblasts and Chinese hamster ovary cells caused substantial susceptibility to FeLV-C but no change in susceptibilities to FeLV-B and other retroviruses. The predicted FLVCR protein contains 555 amino acids and 12 hydrophobic potential membrane-spanning sequences. Database searches indicated that FLVCR is a member of the major-facilitator superfamily of transporters and implied that it may transport an organic anion. RNA blot analyses showed that FLVCR mRNA is expressed in multiple hematopoietic lineages rather than specifically in erythroblasts. These results suggest that the targeted destruction of erythroblasts by FeLV-C may derive from their greater sensitivity to this virus rather than from a preferential susceptibility to infection.Domestic cats infected with the horizontally transmitted feline leukemia virus subgroup A (FeLV-A) often produce mutants (termed FeLV-C) that bind to a distinct cell surface receptor and cause severe aplastic anemia in vivo and erythroblast destruction in bone marrow cultures. The major determinant for FeLV-C-induced anemia has been mapped to a small region of the surface envelope glycoprotein that is responsible for its receptor binding specificity. Thus, erythroblast destruction may directly or indirectly result from FeLV-C binding to its receptor. To address these issues, we functionally cloned a putative cell surface receptor for FeLV-C (FLVCR) by using a human T-lymphocyte cDNA library in a retroviral vector. Expression of the 2.0-kbp FLVCR cDNA in naturally resistant Swiss mouse fibroblasts and Chinese hamster ovary cells caused substantial susceptibility to FeLV-C but no change in susceptibilities to FeLV-B and other retroviruses. The predicted FLVCR protein contains 555 amino acids and 12 hydrophobic potential membrane-spanning sequences. Database searches indicated that FLVCR is a member of the major-facilitator superfamily of transporters and implied that it may transport an organic anion. RNA blot analyses showed that FLVCR mRNA is expressed in multiple hematopoietic lineages rather than specifically in erythroblasts. These results suggest that the targeted destruction of erythroblasts by FeLV-C may derive from their greater sensitivity to this virus rather than from a preferential susceptibility to infection.
Author Willett, B.J
Kabat, D
Tailor, C.S
AuthorAffiliation Department of Biochemistry and Molecular Biology, Oregon Health Sciences University, Portland, Oregon 97201-3098, 1 and Department of Veterinary Pathology, University of Glasgow, Glasgow G61 1QH, United Kingdom 2
AuthorAffiliation_xml – name: Department of Biochemistry and Molecular Biology, Oregon Health Sciences University, Portland, Oregon 97201-3098, 1 and Department of Veterinary Pathology, University of Glasgow, Glasgow G61 1QH, United Kingdom 2
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/10400745$$D View this record in MEDLINE/PubMed
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Corresponding author. Mailing address: Department of Biochemistry and Molecular Biology, Oregon Health Sciences University, 3181 SW Sam Jackson Park Rd., Mail Code L224, Portland, OR 97201-3098. Phone: (503) 494-2548. Fax: (503) 494-8393. E-mail: tailorc@ohsu.edu and kabat@ohsu.edu.
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Snippet Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
Domestic cats infected with the horizontally transmitted feline leukemia virus subgroup A (FeLV-A) often produce mutants (termed FeLV-C) that bind to a...
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StartPage 6500
SubjectTerms 3T3 Cells
Amino Acid Sequence
Anemia, Aplastic
Anemia, Aplastic - virology
Animals
Base Sequence
Caenorhabditis elegans
Carrier Proteins
Carrier Proteins - chemistry
Carrier Proteins - classification
Carrier Proteins - genetics
Cats
chemistry
CHO Cells
classification
complementary DNA
Cricetinae
DNA, Complementary
Feline leukemia virus
genbank/af18637
Gene Expression
genetics
Humans
Leukemia Virus, Feline
Leukemia Virus, Feline - metabolism
metabolism
Mice
Molecular Sequence Data
nucleotide sequences
receptors
Receptors, Virus
Receptors, Virus - chemistry
Receptors, Virus - classification
Receptors, Virus - genetics
Sequence Homology, Amino Acid
T-lymphocytes
Tissue Distribution
virology
Virus-Cell Interactions
Title putative cell surface receptor for anemia-inducing feline leukemia virus subgroup C is a member of a transporter superfamily
URI http://jvi.asm.org/content/73/8/6500.abstract
https://www.ncbi.nlm.nih.gov/pubmed/10400745
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https://www.proquest.com/docview/48664514
https://www.proquest.com/docview/69887716
https://pubmed.ncbi.nlm.nih.gov/PMC112732
Volume 73
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