ライフサイエンスコーパス: reverse transcript

1 gly correlated with the levels of viral late reverse transcripts.

2 deamination of cytidine residues in nascent reverse transcripts.

3 T cells leads to accumulation of incomplete reverse transcripts.

4 ole in retroviral defense by acting on viral reverse transcripts.

5 IAV), and inhibits the accumulation of viral reverse transcripts.

6 utant and induces extensive editing of HIV-1 reverse transcripts.

7 activity, producing overlapping forward and reverse transcripts.

8 unodeficiency virus (HIV-1), and hypermutate reverse transcripts.

9 P virus-like particles and does not edit IAP reverse transcripts.

10 deoxyuridine on the minus strand of nascent reverse transcripts.

11 mutations in both wild-type and Deltavif SIV reverse transcripts.

12 of infection deaminate the newly synthesized reverse transcripts.

13 the ability of those virions to give rise to reverse transcripts.

14 ytes by HIV-1 results in incomplete, labile, reverse transcripts.

15 the cytosolic accumulation of incomplete HIV reverse transcripts.

16 ocked transposition but not the synthesis of reverse transcripts.

17 cts in transposition produced low amounts of reverse transcripts.

18 n that is independent of the accumulation of reverse transcripts.

19 ytes by HIV-1 results in incomplete, labile, reverse transcripts.

20 uced formation of both initial and completed reverse transcripts.

21 incorporate into, and irreversibly terminate reverse transcripts.

22 ntitative PCR revealed normal levels of late reverse transcripts, a moderate reduction of 2-long term

23 roviral factors that can hypermutate nascent reverse transcripts and inhibit the replication of human

24 deamination of cytidine residues in nascent reverse transcripts and inhibiting reverse transcription

25 cytes by HIV-1 results in incomplete, labile reverse transcripts and lack of viral progeny formation.

26 eper resting state, resulting in fewer HIV-1 reverse transcripts and lower IFI16 expression.

27 llers resulted in a marked increase of viral reverse transcripts and mRNA production and led to highe

28 their ability to prevent the accumulation of reverse transcripts and not with the induction of hyperm

29 plementarity resulted in increased levels of reverse transcripts and Tf1 transposition.

30 teration in ratios between intravirion HIV-1 reverse transcripts and viral genomic RNA directly refle

31 g cells, and induce extensive editing of IAP reverse transcripts, APOBEC3A fails to package detectabl

32 osition correlated with reduced level of Tf1 reverse transcripts as determined by DNA blot analysis.

33 ith the RH mutations produced high levels of reverse transcripts, as determined by recombination and

34 educe the frequency of abasic sites in viral reverse transcripts at uracil residues caused by APOBEC3

35 ellular protein that deaminates minus-strand reverse transcript cytosines to uracils.

36 CR experiments revealed that the quantity of reverse transcripts detected in target cells, rather tha

37 ircles, which are formed in the nucleus when reverse transcripts do not integrate, were increased aft

38 cation of retroviruses, yet >/= 90% of HIV-1 reverse transcripts fail to integrate, resulting in accu

39 Here we show that HIV reverse transcripts generated in primary human immune ce

40 e therapy in vivo, the levels of intravirion reverse transcripts have been demonstrated to be dramati

41 Intravirion reverse transcripts have been identified in the blood pl

42 everely impaired in their ability to produce reverse transcripts in infectivity assays.

43 antitative PCR quantitation of SIV and HIV-1 reverse transcripts in newly infected macrophages showed

44 Our results support a role for reverse transcripts in promoting chromosome rearrangemen

45 y to catalyze C-->U deamination of the viral reverse transcripts in the next round of infection.

46 Analysis of the reverse transcripts indicated that the bulk of reverse t

47 zyme complex whose assembly on nascent viral reverse transcripts initiates with A3G dimers binding to

48 , we show how upstream sensing of retroviral reverse transcripts integrates with the downstream effec

49 cofactor LEDGF to effectively integrate the reverse transcript into a host cell chromosome.

50 n (IN) that is required for the insertion of reverse transcripts into the genome of host cells.

51 nt selective pressures, we propose that a TR reverse transcript is mutagenized, integrated into VR as

52 emonstrate that the formation of intravirion reverse transcripts is a dynamic process in vivo.

53 f-life of full-length, integration-competent reverse transcripts is only 1 day.

54 We previously demonstrated that a reverse transcript of a cellular reporter gene (his3-AI)

55 gh rate of dC to dU mutations in the nascent reverse transcripts of HIV that leads to the degradation

56 idence is presented for the presence of cDNA reverse transcripts of the TCR alpha-chain within the hy

57 by quantitative real-time PCR assay of early reverse transcripts or by measurements of virion product

58 fusion and uncoating to occur, the number of reverse transcripts per target cell was similarly enhanc

59 -2 was analyzed by an ELISA spot assay and a reverse transcript polymerase chain reaction method.

60 Furthermore, we found that primary HIV-1 reverse transcripts represented the predominant viral cy

61 Surprisingly, sequencing of the reverse transcripts slowly formed in unstimulated CD4+ T

62 levels of full-length or nearly full-length reverse transcripts than virions isolated from periphera

63 in 2 h of infection and that the turnover of reverse transcripts that occurs in these vif-deficient i

64 e, we show that APOBEC3 limits the levels of reverse transcripts that trigger cytosolic sensing, and

65 deaminase APOBEC3G (A3G), the proportion of reverse transcripts that undergo suicidal autointegratio

66 t of active polymerase reduced the number of reverse transcripts that were initiated and also reduced

67 ed to reduce RNase H activity, the number of reverse transcripts that were initiated was reduced; the

68 ation in human immunodeficiency virus type 1 reverse transcripts unless its incorporation into virion

69 he stability and functionality of these full reverse transcripts, we used an HIV-1 reporter virus tha

70 The intravirion reverse transcripts were also documented to rebound to t

71 Since the levels of intravirion reverse transcripts were altered according to the suscep

72 or instability of the incoming nascent viral reverse transcripts, which could account for the Vif-def