ライフサイエンスコーパス: viroplasm

1 microenvironments called virus factories or 'viroplasm'.

2 NA (dsRNA) genome in viral inclusion bodies (viroplasms).

3 in assembly of viral replication factories (viroplasms).

4 ion with the accumulation of dense masses of viroplasm.

5 e structures formed in addition to masses of viroplasm.

6 were replaced by large, dense aggregates of viroplasm.

7 ) protein is present in small amounts in the viroplasm.

8 n bodies, commonly called viral factories or viroplasms.

9 uctural proteins that normally accumulate in viroplasms.

10 e of plus-strand RNAs for dsRNA synthesis in viroplasms.

11 troduced into the cytosol do not localize to viroplasms.

12 e cytosol that transport plus-strand RNAs to viroplasms.

13 that plus-strand RNAs are synthesized within viroplasms.

14 the relationship between virus factories and viroplasm and the cellular structures that house them.

15 We found that VP1L138P-GFP localized to viroplasms and interacted with NSP2 and/or NSP5 at 31 de

16 virus factories with abnormal electron-dense viroplasms and intermediate density regions associated w

17 d enterocytes and enteroendocrine cells, and viroplasms and lipid droplets are induced.

18 a component of viral replication factories (viroplasms); and VP7, an outer capsid protein, respectiv

19 tion, recruitment of viral proteins into the viroplasms, and possibly genome replication.

20 As viroplasms mature, dNSP2 remains in viroplasms, and the amount of diffuse cytoplasmic dNSP2

21 trand RNAs templating dsRNA synthesis within viroplasms are not susceptible to siRNA-induced RNase de

22 ose that plus-strand RNAs synthesized within viroplasms are the primary source of templates for genom

23 P5; however, the specific role(s) of NSP2 in viroplasm assembly remains largely unknown.

24 P2, one of two rotavirus proteins needed for viroplasm assembly, possesses NTPase, RNA-binding, and h

25 ly has a role subsequent to the formation of viroplasms, consistent with its suspected involvement in

26 rm spherical immature virions, which enclose viroplasm consisting of proteins destined to form the co

27 th vesicles and tubules near masses of dense viroplasm during abortive infection in the absence of th

28 lized for homeostasis of nucleotide pools in viroplasms during genome replication.

29 except for their location at a distance from viroplasm; empty immature virions; and an absence of mat

30 ed that the A30L protein was associated with viroplasm enclosed by crescent and immature virion membr

31 a nonstructural protein, NSP2, essential for viroplasm formation and genome replication/packaging.

32 cleotidyl phosphatase activity is central to viroplasm formation and RNA replication.

33 m-forming proteins guides the specificity of viroplasm formation and, possibly, reassortment restrict

34 The NSP5 protein is required for viroplasm formation during rotavirus infection and is hy

35 roup C NSP2 failed to rescue replication and viroplasm formation in NSP2-deficient cells infected wit

36 To study viroplasm formation in the context of infection, we char

37 oteins enter the nucleus independently, that viroplasm formation requires homologous N-protein intera

38 r with RNA binding activity, is critical for viroplasm formation with its binding partner, NSP5, and

39 sm-like structures (VLS) and is required for viroplasm formation within infected cells.

40 The loss of NSP2 expression inhibited viroplasm formation, genome replication, virion assembly

41 our studies, which may have implications in viroplasm formation, is that the C-terminal helix of NSP

42 matic activities is a principal regulator of viroplasm formation, recruitment of viral proteins into

43 cluding hypophosphorylated NSP5, to initiate viroplasm formation, while viroplasm maturation includes

44 ble-stranded RNA synthesis without affecting viroplasm formation.

45 s necessary for dsRNA synthesis, but not for viroplasm formation.

46 s suggest that charge complementarity of the viroplasm-forming proteins guides the specificity of vir

47 cells or (ii) in uninfected cells along with viroplasm-forming proteins NSP2 and NSP5.

48 (P), and polymerase (L) proteins form large viroplasms in the nuclei of infected plants.

49 ected cells showed the accumulation of large viroplasm inclusions containing virion core proteins but

50 t membrane segments at the edge of the dense viroplasm increased in number at later times, and some i

51 f N and P results in formation of subnuclear viroplasm-like foci.

52 In addition, viroplasm-like inclusions formed in the nuclei of cells

53 avirus NSP5 protein directs the formation of viroplasm-like structures (VLS) and is required for viro

54 ctural proteins, NSP5 and NSP2, in producing viroplasm-like structures (VLS) were previously evaluate

55 le, we demonstrate that NSs protein can form viroplasm-like structures (VLSs) in infected and transfe

56 ion of NSP5 or to interact with NSP5 to form viroplasm-like structures.

57 green fluorescent protein localization into viroplasm-like structures; however, NSP5 insolubility wa

58 on, including influencing the development of viroplasms, linking genome packaging with particle assem

59 However, NSP4 loss of function suppressed viroplasm maturation and caused a maldistribution of non

60 NSP5, to initiate viroplasm formation, while viroplasm maturation includes phosphorylation of NSP5 an

61 As viroplasms mature, dNSP2 remains in viroplasms, and the

62 contain few replication-assembly factories (viroplasms) or replication intermediates and produce vir

63 actions, and that P protein targeting to the viroplasm requires N-P protein interactions that occur a

64 to viral membranes in juxtaposition with the viroplasm, simultaneously preventing the degradation of

65 s and accumulates in cytoplasmic inclusions (viroplasms), sites of genome RNA replication and the ass

66 g amounts later in infection in the maturing viroplasm, suggesting a conversion of dNSP2 into vNSP2.

67 ome occur in cytoplasmic compartments called viroplasms that form during virus infection and are orch

68 hat dNSP2 is associated with NSP5 in nascent viroplasms that lack vNSP2.

69 Viral inclusion bodies, or viroplasms, that form in rotavirus-infected cells direct

70 h LC3 in cap-like structures associated with viroplasms, the site of nascent viral RNA replication, s

71 protein NSP4 recruits progeny DLPs formed in viroplasms to the ER, where the particles are converted

72 ble crescents and immature virions devoid of viroplasm were seen in place of normal structures.

73 n antiserum specifically labeled the nuclear viroplasms, whereas the M2 antiserum was more generally

74 e separated from the electron-dense granular viroplasm, which accumulated in large spherical masses.

75 crescents, at the surface of dense masses of viroplasm, which were labeled with antibodies to the A11

76 al octamer, is critical for the formation of viroplasms, which are exclusive sites for replication an

77 ake place in specialized compartments called viroplasms, which are formed during infection and involv

78 on affects the ability of VP1 to localize to viroplasms, which are the sites of RV RNA synthesis, by

79 ome occur in cytoplasmic compartments called viroplasms, which form during virus infection.

80 tion occurs in cytoplasmic inclusions called viroplasms whose formation requires the interactions of

81 ed aberrant large, dense, granular masses of viroplasm with clearly defined margins; viral crescent m

82 structures with lucent interiors and foci of viroplasm with dense centers mapped to the A30L open rea

83 s, specifically the association of the dense viroplasm with viral membranes.