Abortive reverse transcription by mutants of Moloney murine leukemia virus deficient in the reverse transcriptase-associated RNase H function.
about
Murine leukemia virus reverse transcriptase: structural comparison with HIV-1 reverse transcriptaseThe Host RNAs in Retroviral ParticlesStructural and Binding Analysis of Pyrimidinol Carboxylic Acid and N-Hydroxy Quinazolinedione HIV-1 RNase H InhibitorsStructural analysis of monomeric retroviral reverse transcriptase in complex with an RNA/DNA hybridRevealing domain structure through linker-scanning analysis of the murine leukemia virus (MuLV) RNase H and MuLV and human immunodeficiency virus type 1 integrase proteinsMultiple nucleotide preferences determine cleavage-site recognition by the HIV-1 and M-MuLV RNases H.Structural determinants of murine leukemia virus reverse transcriptase that affect the frequency of template switchingEffects of homology length in the repeat region on minus-strand DNA transfer and retroviral replication.Replication of phenotypically mixed human immunodeficiency virus type 1 virions containing catalytically active and catalytically inactive reverse transcriptase.Mutants of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase resistant to nonnucleoside reverse transcriptase inhibitors demonstrate altered rates of RNase H cleavage that correlate with HIV-1 replication fitness in cell culture.Y586F mutation in murine leukemia virus reverse transcriptase decreases fidelity of DNA synthesis in regions associated with adenine-thymine tracts.Structural features in the HIV-1 repeat region facilitate strand transfer during reverse transcription.Pervasive genomic recombination of HIV-1 in vivo.The nature of the N-terminal amino acid residue of HIV-1 RNase H is critical for the stability of reverse transcriptase in viral particles.Human immunodeficiency virus type 2 reverse transcriptase activity in model systems that mimic steps in reverse transcription.Mutation of amino acids in the connection domain of human immunodeficiency virus type 1 reverse transcriptase that contact the template-primer affects RNase H activity.Mechanisms and factors that influence high frequency retroviral recombinationUnique progressive cleavage mechanism of HIV reverse transcriptase RNase HEffects on DNA synthesis and translocation caused by mutations in the RNase H domain of Moloney murine leukemia virus reverse transcriptaseReversion of a Moloney murine leukemia virus RNase H mutant at a second site restores enzyme function and infectivitySequence and structural determinants required for priming of plus-strand DNA synthesis by the human immunodeficiency virus type 1 polypurine tract.RNase H domain of Moloney murine leukemia virus reverse transcriptase retains activity but requires the polymerase domain for specificity.Genome-Wide Search for Host Association Factors during Ovine Progressive Pneumonia Virus InfectionRetrovirus variation and reverse transcription: abnormal strand transfers result in retrovirus genetic variation.Replication of the retroviral terminal repeat sequence during in vivo reverse transcription.Apparent defects in processive DNA synthesis, strand transfer, and primer elongation of Met-184 mutants of HIV-1 reverse transcriptase derive solely from a dNTP utilization defect.Dynamic binding orientations direct activity of HIV reverse transcriptasePreferred sequences within a defined cleavage window specify DNA 3' end-directed cleavages by retroviral RNases HExtended minus-strand DNA as template for R-U5-mediated second-strand transfer in recombinational rescue of primer binding site-modified retroviral vectors.Amino acids essential for RNase H activity of hepadnaviruses are also required for efficient elongation of minus-strand viral DNA.Replication errors during in vivo Ty1 transposition are linked to heterogeneous RNase H cleavage sites.Requirements for minus-strand transfer catalyzed by Rous sarcoma virus reverse transcriptase.Utilization of nonhomologous minus-strand DNA transfer to generate recombinant retroviruses.Selected mutations of the duck hepatitis B virus P gene RNase H domain affect both RNA packaging and priming of minus-strand DNA synthesis.Defects in Moloney murine leukemia virus replication caused by a reverse transcriptase mutation modeled on the structure of Escherichia coli RNase H.Transactivation of the minus-strand DNA transfer by nucleocapsid protein during reverse transcription of the retroviral genome.Two defective forms of reverse transcriptase can complement to restore retroviral infectivity
P2860
Q24647519-9356F019-D88B-4422-8C8B-D716728C2EA7Q26739938-05F1C32B-5D09-4DA7-86F7-CD3B99BB40CFQ27667421-38F01853-AF94-4E09-B547-45731DB7E3A0Q27676135-02EA0353-8B66-4199-9519-79C106D12ED3Q33257614-8A64652F-D580-4E59-AFB2-50F818C738A9Q33695787-98746311-B575-46F3-8B62-698B9D4443BAQ33809246-64FD9507-D2AF-4957-A452-583F9844B1EFQ33835531-D41AC97C-9013-41D0-8EE8-D98692ABFEA0Q33843501-1B3543C4-637C-4D45-BC35-016CFA76870AQ33873983-AB00D0FD-8CF9-46E9-97E7-99F6D341E3DBQ34099109-D50F4095-9259-4B34-99DA-90680820D8C8Q34363753-77A07725-9B2A-4DB7-A3CE-CAF94BE9CBBFQ34645720-9B77C50A-7420-4E59-B602-B53AE16076C4Q34991047-EF695B9C-062D-4B1C-BF0C-05784E928E76Q35149625-8B669FE8-324C-464F-B9D6-490C24E750DCQ35155286-C3BE9D8E-CB8D-470D-BC98-6DC66A5C25A4Q35276750-64E8726E-CC09-47B7-8AD3-872DDC64A3B9Q35360809-2412C36E-D0AE-442B-81B4-879FD745F160Q35841879-35053337-4F67-4F55-862B-BA4C536BB332Q35845242-71384DCF-EFBC-493F-B751-61F848E2B765Q35866117-4FDA4E7C-B9D7-48F5-AAFE-419922765500Q35873623-7D5C5F58-237B-41CC-BD62-1753E55509AFQ35948010-E26EE4D2-4A3A-4038-A3A1-BBCABDDCEAECQ36439044-E38064FD-086C-4FC3-9BC8-BEE925718D42Q36650132-A897AB71-829F-4312-9432-7E7B0E422DFCQ36727282-DC50016F-3768-4DDA-A53D-9CEAE9ADAEE6Q37126933-9C19BD28-532E-41C0-A990-583F4A45703FQ37431890-837C2EE4-24F3-46ED-95D2-CACC0A52CC1BQ38339423-F620E6EE-FB99-4BD0-8F9E-C0BB1133DA3FQ38353690-1E6A865A-A345-4B93-8634-6A3505F0B746Q39574404-711E9FC8-5462-45DB-A0BB-2C3D2A2FBE05Q39604595-096DF71A-2A41-4C8E-8FEA-A678617C6FF3Q39878819-D84EB754-7315-402B-8EDD-E53F45D124AEQ40038621-B5050674-4399-4CC2-8F0E-4931ABC3F52FQ40063803-7B1C4630-90A9-4A2F-AC9C-6D27EBD62FA8Q40790993-77A2440E-F873-42FD-ACEE-63BA048EA93BQ40874391-F2AF8A4B-4C01-4AFF-8DA6-17E35B45BB8C
P2860
Abortive reverse transcription by mutants of Moloney murine leukemia virus deficient in the reverse transcriptase-associated RNase H function.
description
1991 nî lūn-bûn
@nan
1991年の論文
@ja
1991年論文
@yue
1991年論文
@zh-hant
1991年論文
@zh-hk
1991年論文
@zh-mo
1991年論文
@zh-tw
1991年论文
@wuu
1991年论文
@zh
1991年论文
@zh-cn
name
Abortive reverse transcription ...... e-associated RNase H function.
@en
type
label
Abortive reverse transcription ...... e-associated RNase H function.
@en
prefLabel
Abortive reverse transcription ...... e-associated RNase H function.
@en
P2093
P2860
P1433
P1476
Abortive reverse transcription ...... e-associated RNase H function.
@en
P2093
P2860
P304
P407
P577
1991-08-01T00:00:00Z