ライフサイエンスコーパス: AMV

1 AMV and ilarvirus coat protein sequence alignment center

2 AMV and TSV coat proteins, which share little primary am

3 AMV RNA 4 and Arabidopsis HSP21 showed only a slight dep

4 AMV RT binds much tighter to template- primer and has a

5 AMV was discovered in the 1930s as a virus that caused a

6 AMV-RT degraded the RNA to segments 11-12 nt long, and r

7 To detect coat-protein-activated AMV RNA replication, we designed and characterized a sub

8 AUGC sequences that are conserved among AMV and ilarvirus RNAs were among the invariant nucleoti

9 tein interactions are highly conserved among AMV and the ilarvirus RNAs.

10 ty with eIF4F, whereas Arabidopsis HSP21 and AMV RNA 4 used both eIF4F and eIF(iso)4F equally well.

11 , although both Rous sarcoma virus (RSV) and AMV could replicate in cultures of either embryonic fibr

12 ned in this myb oncogene were shared between AMV and the avian E26 leukemia virus, but were not conta

13 We found that (th)A is recognized by AMV reverse transcriptase as A, and is deaminated rapidl

14 over twice the length of that synthesized by AMV RT and can synthesize cDNA over 4 times longer than

15 y avian erythroblastosis virus (AEV) than by AMV.

16 First, AMV was used to demonstrate that all oncogenic viruses d

17 ion of an RNA binding consensus sequence for AMV and ilarvirus coat proteins, provides a framework fo

18 replication and may explain why heterologous AMV and ilarvirus coat protein-RNA mixtures are infectio

19 We measured the ability of HIV-, AMV- and MuLV-RT to coordinate DNA-dependent DNA synthes

20 Consistent with these results, HIV-, AMV- and MuLV-RT showed relatively higher affinity for R

21 QRT-SDA) of an HIV gag sequence by including AMV reverse transcriptase, a quantitative control sequen

22 eport the addition of ammonium metavanadate (AMV), a phosphatase inhibitor, to PIA (PIA-AMV) induced

23 ound that when comparing wild-type or mutant AMV RT with the respective M-MLV RT, the avian enzymes r

24 The ability of AMV IN to interact with internal att sequences to mediat

25 In the case of AMV, it was shown that almost the entire retroviral env

26 Furthermore, the BIR domains of AMV-IAP protein were demonstrated to bind the mammalian

27 dual baculoviral IAP repeat (BIR) domains of AMV-IAP was investigated by using a random-peptide, phag

28 understanding the functional equivalence of AMV and TSV coat proteins in binding RNA and activating

29 ity of atALKBH9B affected the infectivity of AMV but not of CMV, correlating with the ability of atAL

30 organization model as an alternate model of AMV replication that offers an improved fit to the avail

31 binding of the 3'-terminal 39 nucleotides of AMV RNA 3/4 (AMV843-881) to an amino-terminal coat prote

32 oth of which contribute to the warm phase of AMV.

33 suggests that the 3' untranslated regions of AMV and ilarvirus RNAs have the potential to fold into p

34 protein's function in the earliest stages of AMV replication.

35 polymerase activity was observed with MLV or AMV reverse transcriptase, T7 DNA polymerase, or DNA pol

36 r), but not that of RTs derived from MMLV or AMV.

37 Alginate induction in PAO1 on PIA-AMV was correlated with increased proteolytic degradatio

38 (AMV), a phosphatase inhibitor, to PIA (PIA-AMV) induced mucoidy in both these laboratory strains an

39 st a model of alginate induction and the PIA-AMV medium may be suitable for examining early lung colo

40 a moorei entomopoxvirus-encoded IAP protein (AMV-IAP).

41 For this reason AMV was often used as a prototypic retrovirus in order t

42 can synthesize cDNA over 4 times longer than AMV RT in assays with poly(rA) templates.

43 the conformational switch model states that AMV coat protein blocks minus-strand RNA synthesis, whil

44 Here, the AMV coat protein RNA binding domain is shown to contain

45 eased the relative abundance of m(6)A in the AMV genome, impairing the systemic invasion of the plant

46 ich amino-terminal RNA binding domain of the AMV coat protein lacks previously identified RNA binding

47 myeloblastosis virus reverse transcriptase (AMV-RT) or human DNA polymerase beta (pol beta), was sig

48 ale Atlantic multidecadal ocean variability (AMV), including the extreme pre-greenhouse-gas northern

49 ecrosis virus RNA, and alfalfa mosaic virus (AMV) 4, were used in wheat germ in vitro translation ass

50 e Bromoviridae family, alfalfa mosaic virus (AMV) and cucumber mosaic virus (CMV).

51 Alfalfa mosaic virus (AMV) and ilarvirus RNAs are infectious only in the prese

52 A defining feature of alfalfa mosaic virus (AMV) and ilarviruses [type virus: tobacco streak virus (

53 The coat proteins of alfalfa mosaic virus (AMV) and the related ilarviruses bind specifically to th

54 Alfalfa mosaic virus (AMV) coat protein and tobacco streak virus (TSV) coat pr

55 scribing regulation of alfalfa mosaic virus (AMV) replication have been tested using biochemical assa

56 The alfalfa mosaic virus (AMV) RNAs are infectious only in the presence of the vir

57 three genomic RNAs of Alfalfa mosaic virus (AMV).

58 type recombinant avian myeloblastosis virus (AMV) and Moloney murine leukemia virus (M-MLV) reverse t

59 ts with purified avian myeloblastosis virus (AMV) IN and retrovirus-like donor substrates containing

60 oncogene of the avian myeloblastosis virus (AMV) is unique among known oncogenes in that it causes o

61 , encoded by the avian myeloblastosis virus (AMV), can induce acute monoblastic leukemia in vivo and

62 d retroviral RT, avian myeloblastosis virus (AMV).

63 r Hid-induced cell death was suppressed when AMV-IAP was coexpressed.

64 RSV could transform only fibroblasts whereas AMV could transform only hematopoietic cells.

65 a 2:1 preference to insert dA over dC, while AMV-RT incorporated predominantly dC.

66 Second, chickens infected with AMV develop remarkably high white counts and therefore t

67 m and Hid were demonstrated to interact with AMV-IAP in vivo, and Grim- or Hid-induced cell death was