scholarly journals The Entire Nucleotide Sequence of Friend-Related and Paralysis-Inducing PVC-441 Murine Leukemia Virus (MuLV) and Its Comparison with Those of PVC-211 MuLV and Friend MuLV

1998 ◽  
Vol 72 (4) ◽  
pp. 3423-3426 ◽  
Author(s):  
Atsushi Tanaka ◽  
Kiyomasa Oka ◽  
Keiji Tanaka ◽  
Atsushi Jinno ◽  
Sandra K. Ruscetti ◽  
...  
Keyword(s):  
Nucleotide Sequence ◽  
Murine Leukemia Virus ◽  
Chinese Hamster Ovary Cells ◽  
Leukemia Virus ◽  
Chinese Hamster ◽  
Brain Capillary Endothelial Cell ◽  
Ovary Cells ◽  
The Difference ◽  
Entire Nucleotide Sequence ◽  
Murine Leukemia

ABSTRACT PVC-441 murine leukemia virus (MuLV) is a member of the PVC group of Friend MuLV (F-MuLV)-derived neuropathogenic retroviruses. In order to determine the molecular basis for the difference in neuropathogenicity between PVC-441 and the previously characterized PVC-211 MuLVs, the entire nucleotide sequence of PVC-441 MuLV was determined and compared with those of PVC-211 and F-MuLV. The results suggest that PVC-441 and PVC-211 MuLVs were formed as a result of random mutations of F-MuLV and developed differently. The distinct pathogenicities of PVC-441 and PVC-211 MuLVs were maintained in the viruses regenerated from their molecular clones, and the sequences responsible for the pathological differences observed can be localized to the env gene. The amino acid sequence of PVC-441 deduced from its nucleotide sequence revealed a number of differences from PVC-211, the most striking of which was a difference at position 129 of the SU proteins in the two viruses. Host range studies with a brain capillary endothelial cell line (RTEC-6) and Chinese hamster ovary cells (CHO-K1) revealed that PVC-441, like PVC-211, could infect these cells but its efficiency of infection was lower than that of PVC-211. These results may account for the difference in neuropathogenicity between PVC-441 and PVC-211.

scholarly journals Isolation of Cell Lines That Show Novel, Murine Leukemia Virus-Specific Blocks to Early Steps of Retroviral Replication

2005 ◽  
Vol 79 (20) ◽  
pp. 12969-12978 ◽  
Author(s):  
James W. Bruce ◽  
Kenneth A. Bradley ◽  
Paul Ahlquist ◽  
John A. T. Young
Keyword(s):  
Cell Lines ◽  
Reverse Transcription ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Mutant Cell ◽  
Chinese Hamster ◽  
High Volume ◽  
Early Stages ◽  
Retroviral Replication ◽  
Murine Leukemia

ABSTRACT In order to identify cellular proteins required for early stages of retroviral replication, a high volume screening with mammalian somatic cells was performed. Ten pools of chemically mutagenized Chinese hamster ovary (CHO-K1) cells were challenged with a murine leukemia virus (MLV) vector pseudotyped with the vesicular stomatitis virus glycoprotein (VSV-G), and cells that failed to be transduced were enriched by cell sorting. Each pool yielded a clonally derived cell line with a 5-fold or greater resistance to virus infection, and five cell lines exhibited a >50-fold resistance. These five cell lines were efficiently infected by a human immunodeficiency virus vector pseudotyped with VSV-G. When engineered to express the TVA receptor for subgroup A avian sarcoma and leukosis virus (ASLV-A), the five cell lines were resistant to infection with a MLV vector pseudotyped with the ASLV-A envelope protein but were fully susceptible to infection with an ASLV-A vector. Thus, the defect in these cells resides after virus-cell membrane fusion and, unlike those in other mutant cell lines that have been described, is specific for the MLV core. To identify the specific stages of MLV infection that are impaired in the resistant cell lines, real-time quantitative PCR analyses were employed and two phenotypic groups were identified. Viral infection of three cell lines was restricted before reverse transcription; in the other two cell lines, it was blocked after reverse transcription, nuclear localization, and two-long terminal repeat circle formation but before integration. These data provide genetic evidence that at least two distinct intracellular gene products are required specifically for MLV infection. These cell lines are important tools for the biochemical and genetic analysis of early stages in retrovirus infection.

Nucleotide Sequence of a Cloned Murine Leukemia Virus DNA Fragment

1980 ◽  
Vol 44 (0) ◽  
pp. 1275-1279
Author(s):  
J. G. Sutcliffe ◽  
T. M. Shinnick ◽  
R. A. Lerner ◽  
P. Johnson ◽  
I. M. Verma
Keyword(s):  
Nucleotide Sequence ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Dna Fragment ◽  
Murine Leukemia

scholarly journals Complete nucleotide sequence of a neuropathogenic variant of Friend murine leukemia virus PVC-211

1992 ◽  
Vol 20 (12) ◽  
pp. 3249-3249 ◽  
Author(s):  
Mary P. Remington ◽  
Paul M. Hoffman ◽  
Sandra K. Ruscetti ◽  
Michiaki Masuda
Keyword(s):  
Nucleotide Sequence ◽  
Murine Leukemia Virus ◽  
Complete Nucleotide Sequence ◽  
Leukemia Virus ◽  
Murine Leukemia

scholarly journals Nucleotide sequence of the 3' end of MCF 247 murine leukemia virus.

1983 ◽  
Vol 45 (1) ◽  
pp. 291-298 ◽  
Author(s):  
M Kelly ◽  
C A Holland ◽  
M L Lung ◽  
S K Chattopadhyay ◽  
D R Lowy ◽  
...  
Keyword(s):  
Nucleotide Sequence ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Murine Leukemia

scholarly journals Identification of an Extracellular Domain within the Human PiT2 Receptor That Is Required for Amphotropic Murine Leukemia Virus Binding

2004 ◽  
Vol 78 (2) ◽  
pp. 595-602 ◽  
Author(s):  
Steven A Feldman ◽  
Karen B. Farrell ◽  
Ravi K. Murthy ◽  
Jill L. Russ ◽  
Maribeth V. Eiden
Keyword(s):  
Murine Leukemia Virus ◽  
Sodium Phosphate ◽  
Leukemia Virus ◽  
Chinese Hamster ◽  
Extracellular Domain ◽  
Virus Binding ◽  
Type Iii ◽  
Amphotropic Murine Leukemia Virus ◽  
Critical Residue ◽  
Murine Leukemia

ABSTRACT Human PiT2 (PiT2) is a multiple-membrane-spanning protein that functions as a type III sodium phosphate cotransporter and as the receptor for amphotropic murine leukemia virus (A-MuLV). Human PiT1 (PiT1), another type III sodium phosphate cotransporter, is a highly related protein that functions as a receptor for gibbon ape leukemia virus but not for A-MuLV. The ability of PiT1 and PiT2 to function as discrete viral receptors with unique properties presumably is reflected in critical residue differences between these two proteins. Early efforts to map the region(s) within PiT2 that is important for virus binding and/or entry relied on infection results obtained with PiT1-PiT2 chimeric cDNAs expressed in Chinese hamster ovary (CHOK1) cells. These attempts to localize the PiT2 virus-binding site were hampered because they were based on infectivity, not binding, assays, and therefore, receptors that bound but failed to facilitate virus entry could not be distinguished from receptors that did not bind virus. Using a more accurate topological model for PiT2 as well as an A-MuLV receptor-binding assay, we have identified extracellular domain one (ECD1) of the human PiT2 receptor as being important for A-MuLV binding and infection.

Regulation of Na+/Ca2+exchange activity by cytosolic Ca2+ in transfected Chinese hamster ovary cells

1998 ◽  
Vol 275 (1) ◽  
pp. C50-C55 ◽  
Author(s):  
Yu Fang ◽  
Madalina Condrescu ◽  
John P. Reeves
Keyword(s):  
Chinese Hamster Ovary ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Hill Coefficient ◽  
Acetoxymethyl Ester ◽  
Ovary Cells ◽  
Whole Cells ◽  
Order Of Magnitude ◽  
The Difference ◽  
Exchange Activity

Transfected Chinese hamster ovary cells stably expressing the bovine cardiac Na+/Ca2+exchanger (CK1.4 cells) were used to determine the range of cytosolic Ca2+ concentrations ([Ca2+]i) that activate Na+/Ca2+exchange activity. Ba2+ influx was measured in fura 2-loaded, ionomycin-treated cells under conditions in which the intracellular Na+concentration was clamped with gramicidin at ∼20 mM. [Ca2+]iwas varied by preincubating ionomycin-treated cells with either the acetoxymethyl ester of EGTA or medium containing 0–1 mM added CaCl2. The rate of Ba2+ influx increased in a saturable manner with [Ca2+]i, with the half-maximal activation value of 44 nM and a Hill coefficient of 1.6. When identical experiments were carried out with cells expressing a Ca2+-insensitive mutant of the exchanger, Ba2+influx did not vary with [Ca2+]i. The concentration for activation of exchange activity was similar to that reported for whole cardiac myocytes but approximately an order of magnitude lower than that reported for excised, giant patches. The reason for the difference in Ca2+regulation between whole cells and membrane patches is unknown.

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