Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.27.3 (RNase T1)
 1,228 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A group of mink cell focus-forming (MCF) viruses was derived by inoculation of NFS/N mice with Moloney murine leukemia virus (Mo-MuLV 1387) and was compared to a similarly derived group of MCF viruses from mice inoculated with Friend MuLV (Fr-MuLV 57). Antigenic analyses using monoclonal antibodies specific for MCF virus and xenotropic MuLV envelope proteins and genomic structural analyses by RNase T1-resistant oligonucleotide finger-printing indicated that the Moloney and Friend MCF viruses arose by recombination of the respective ecotropic MuLVs with different endogenous retrovirus sequences of NFS mice.
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PMID:Friend and Moloney murine leukemia viruses specifically recombine with different endogenous retroviral sequences to generate mink cell focus-forming viruses. 257 66

Friend murine leukemia helper viruses (F-MuLV) 57 and B3 were indistinguishable by genomic structural analyses with RNase T1-resistant oligonucleotide fingerprinting and by antigenic reactivity with a panel of 31 monoclonal antibodies directed against murine leukemia viruses. Nevertheless, F-MuLV 57 and B3 had strikingly different virulences. Approximately 2 months after inoculation, IRW and NFS/N mice inoculated as newborns with F-MuLV 57 had gross splenomegaly caused by erythroid proliferation. In contrast, an equivalent dose of F-MuLV B3 induced spleen or lymph node enlargement 4 to 13 months after inoculation. Although most cases of spleen enlargement in F-MuLV B3-inoculated mice were due to erythroid proliferation, lymphoid or myeloid proliferation was also frequently observed. The replication of both F-MuLV 57 and B3 was equally efficient, and both viruses generated recombinant dual-tropic mink cell focus-forming (MCF) viruses with the same kinetics and efficiency. Moreover, MCF viruses induced by F-MuLV 57 and B3 had the same antigenic patterns. Therefore, the ability of F-MuLV to induce early splenomegaly did not correlate with the generation of recombinant MCF viruses.
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PMID:Analysis of two strains of Friend murine leukemia viruses differing in ability to induce early splenomegaly: lack of relationship with generation of recombinant mink cell focus-forming viruses. 300 61

SL3-3 is a leukemogenic, ecotropic retrovirus produced by a T-cell line derived from a spontaneous lymphoma of an AKR mouse. We have isolated a molecular clone of its DNA provirus from infected NIH 3T3 fibroblasts. Cloned proviral DNA produced infectious virus upon transfection onto NIH 3T3 cells. Virus derived by transfection induced lymphomas at high frequency in AKR/J, C3H(f)/Bi, CBA/J, and NFS/N mice. Heteroduplex and RNase T1 fingerprinting analyses showed that the genomes of SL3-3 and the non-leukemogenic virus, Akv, contain no major substitutions relative to one another and differ by only a few base changes. These results unambiguously show that SL3-3 is a highly leukemogenic virus and that major rearrangements of the genome relative to Akv are not required for virulence.
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PMID:Molecular cloning of a highly leukemogenic, ecotropic retrovirus from an AKR mouse. 629 72

A family of recombinant mink cell focus-forming viruses (MCF) was derived by inoculation of NFS mice with a Friend murine leukemia virus, and their genomes were analyzed by RNase T1-resistant oligonucleotide fingerprinting. The viruses were obtained from the thymuses and spleens of preleukemic and leukemic animals and were evaluated for dualtropism and oncogenicity. All these isolates induced cytopathic foci on mink cells but could be classified into two groups based on their relative infectivities for SC-1 (mouse) or mink (ATCC CCL64) cells. One group of Friend MCFs (F-MCFs) (group I) exhibited approximately equal infectivities for SC-1 and mink cells, whereas a second group (group II) infected mink cells 1,000- to 10,000-fold more efficiently than SC-1 cells. Structural analyses of the F-MCFs revealed that group I and group II viruses correlated with recombination of Friend murine leukemia virus with two distinct, but closely related, endogenous NFS proviral sequences. No correlation was found between the type of F-MCF and the tissue of origin or the disease state of the animal. Furthermore, none of the F-MCF isolates were found to be oncogenic in NFS/N or AKR/J mice. F-MCFs of both groups underwent extensive substitution of ecotropic sequences, involving much of the gag and env genes of group I F-MCFs and most of the gag, pol, and env genes of group II F-MCFs. All F-MCF isolates retained the 3' terminal U3 region of Friend murine leukemia virus. Comparison of the RNAs of the F-MCFs with RNAs of MCFs derived from NFS.Akv-1 or NFS.Akv-2 mice indicated that the F-MCFs were derived from NFS proviral sequences which are distinct from the sequences contained in NFS.Akv MCF isolates. This result suggested that recombination with particular endogenous proviral sequences to generate MCFs may be highly specific for a given murine leukemia virus.
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PMID:Generation of mink cell focus-forming viruses by Friend murine leukemia virus: recombination with specific endogenous proviral sequences. 642 51