ArticleJournal of virology1997
Mutational analysis of the proposed gibbon ape leukemia virus binding site in Pit1 suggests that other regions are important for infection.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 19 citations in OpenAlex.
- Endogenous Gibbon Ape Leukemia Virus Identified in a Rodent (Melomys burtoni subsp.) from Wallacea (Indonesia).Journal of virology · 2016Article
- New structural arrangement of the extracellular regions of the phosphate transporter SLC20A1, the receptor for gibbon ape leukemia virus.The Journal of biological chemistry · 2009Article
- The central half of Pit2 is not required for its function as a retroviral receptor.Journal of virology · 2004Article
- Identification of an extracellular domain within the human PiT2 receptor that is required for amphotropic murine leukemia virus binding.Journal of virology · 2004Article
- Genetic and biochemical analyses of receptor and cofactor determinants for T-cell-tropic feline leukemia virus infection.Journal of virology · 2002Article
- Reassessing the role of region A in Pit1-mediated viral entry.Journal of virology · 2002Article
- Fusion-defective gibbon ape leukemia virus vectors can be rescued by homologous but not heterologous soluble envelope proteins.Journal of virology · 2002Article
- Feline Pit2 functions as a receptor for subgroup B feline leukemia viruses.Journal of virology · 2001Article
- Transmembrane topology of PiT-2, a phosphate transporter-retrovirus receptor.Journal of virology · 2001Article
- A 13-amino-acid Pit1-specific loop 4 sequence confers feline leukemia virus subgroup B receptor function upon Pit2.Journal of virology · 2000Article
- Amphotropic murine leukemia virus entry is determined by specific combinations of residues from receptor loops 2 and 4.Journal of virology · 1999Article
- Gibbon ape leukemia virus receptor functions of type III phosphate transporters from CHOK1 cells are disrupted by two distinct mechanisms.Journal of virology · 1999Article
- The second extracellular loop of CXCR4 determines its function as a receptor for feline immunodeficiency virus.Journal of virology · 1998Article
- Entry of amphotropic murine leukemia virus is influenced by residues in the putative second extracellular domain of its receptor, Pit2.Journal of virology · 1998Article
- Single amino acid insertion in loop 4 confers amphotropic murine leukemia virus receptor function upon murine Pit1.Journal of virology · 1998Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Region A of Pit1 (residues 550 to 558 in domain IV) and related receptors has remained the only sequence implicated in gibbon ape leukemia virus (GALV) infection, and an acidic residue at the first position appeared indispensable. The region has also been proposed to be the GALV binding site, but this lacks empirical support. Whether an acidic residue at the first position in this sequence is a definitive requirement for GALV infection has also remained unclear; certain receptors retain function even in the absence of this acidic residue. We report here that in Pit1 an acidic residue is dispensable not only at position 550 but also at 553 alone and at both positions. Further, the virus requires no specific residue at either position. Mutations generated a collection of region A sequences, often with fundamentally different physicochemical properties (overall hydrophobicity or hydrophilicity and net charge of -1, or 0, or +1), and yet Pit1 remained an efficient GALV receptor. A comparison of these sequences and a few previously published ones from highly efficient GALV receptors revealed that every position in region A can vary without affecting GALV entry. Even Pit2 is nonfunctional for GALV only because it has lysine at the first position in its region A, which is otherwise highly diverse from region A of Pit1. We propose that region A itself is not the GALV binding motif and that other sequences are required for virus entry. Indeed, certain Pit1/Pit2 chimeras revealed that sequences outside domain IV are specifically important for GALV infection.
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