ライフサイエンスコーパス: nuclear inclusion

1 ed by large intranuclear protein aggregates (nuclear inclusions).

2 accumulates in a single, ubiquitin-positive nuclear inclusion.

3 tion but increase the fraction of cells with nuclear inclusions.

4 g its sequestration away from promoters into nuclear inclusions.

5 omoted the accumulation of mutant ATXN7 into nuclear inclusions.

6 y by the presence of neuropil aggregates and nuclear inclusions.

7 to aggregate and form larger cytoplasmic or nuclear inclusions.

8 th AR species but not to fragment-containing nuclear inclusions.

9 plicing defects in the absence of detectable nuclear inclusions.

10 redistributed Sp100 to mutant ataxin-1[82Q] nuclear inclusions.

11 Hsp70 decreases the percentage of cells with nuclear inclusions.

12 val lethality, but not neuronal apoptosis or nuclear inclusions.

13 ese neurons weeks prior to the appearance of nuclear inclusions.

14 n of the protein, with large cytoplasmic and nuclear inclusions.

15 ensity of such cells to form cytoplasmic and nuclear inclusions.

16 ence the appearance or frequency of neuronal nuclear inclusions.

17 ost CBP was not co-localized with huntingtin nuclear inclusions.

18 om the depletion of transcription factors by nuclear inclusions.

19 oduced from the mutant allele is retained in nuclear inclusions.

20 huntingtin, but not normal huntingtin, forms nuclear inclusions.

21 eractive and that contain paramyxovirus-like nuclear inclusions.

22 med vacuoles and filamentous cytoplasmic and nuclear inclusions.

23 XN1 colocalized and interacted with ATXN1 in nuclear inclusions.

24 that relies on the tobacco etch virus (TEV) nuclear inclusion a (NIa) protease and leads to the coor

25 The WSMV NIb-CP junction containing the nuclear inclusion a (NIa) protease cleavage site was dup

26 e have shown that the protease domain of the nuclear inclusion a protease (NIaPro) from PVY is the el

27 ed that production of a single TuMV protein, Nuclear Inclusion a-Protease (NIa-Pro) domain, was respo

28 Production of a single TuMV protein, nuclear inclusion a-protease domain (NIa-Pro), increased

29 These fragments constituted neuronal nuclear inclusions and appeared before neurological symp

30 give rise to repeat expansion RNAs that form nuclear inclusions and compromise the function of myonuc

31 ainst neuronal dysfunction for polyglutamine nuclear inclusions and exclude significant impairment of

32 he toxic RNA is associated with formation of nuclear inclusions and late-onset degenerative changes i

33 Hallmark features of HD, including nuclear inclusions and neuropil aggregates, were observe

34 lation of the mutant Atxn3 protein, abundant nuclear inclusions and, in select brain regions, extranu

35 r membrane blebbing, mitochondrial swelling, nuclear inclusions, and absence of junctional end feet.

36 in nuclear protein aggregation, filamentous nuclear inclusions, and an increase in cell death.

37 on and had tubulointerstitial nephritis with nuclear inclusions, apoptosis, and progressive destructi

38 in HD postmortem brains and by the fact that nuclear inclusions are only detected by antibodies to th

39 -glucuronidase (GUS) were placed between the nuclear inclusion b (NIb) and coat protein (CP) domains

40 no acid sequence of the potato virus Y (PVY) nuclear inclusion b protein is highly homologous to the

41 rganize the VICE domain component Hsc70 into nuclear inclusion bodies that resemble VICE domains.

42 Renal lead-containing nuclear inclusion bodies were frequently observed in WT

43 HDAC4) and MEF2 and colocalizes with them in nuclear inclusion bodies.

44 a large heterogeneity in the dynamics of the nuclear inclusions compared with the compact and immobil

45 c ganglion cells in PrP-SCA7-92Q mice harbor nuclear inclusions composed of transgene-derived ataxin-

46 Nuclear inclusions contained primarily cleaved N-termina

47 the anti-polyP and anti-C terminus mAbs bind nuclear inclusions containing htt.

48 Nuclear inclusions containing polyQ-expanded htt recruit

49 Nuclear inclusions did not appear until 18 months.

50 tant Arx in mouse brains results in neuronal nuclear inclusion formation.

51 icity on the proteins and is associated with nuclear inclusion formation.

52 ell signaling cascades, is incorporated into nuclear inclusions formed by polyglutamine-containing pr

53 tamine protein, ataxin-3, and establish that nuclear inclusions formed by this protein are aggregates

54 We also show CBP incorporation into nuclear inclusions formed in a cell culture model of ano

55 hich aggregate into neuronal cytoplasmic and nuclear inclusions in affected patients, however their c

56 ent of several non-neuronal tissues revealed nuclear inclusions in hepatocytes and choroid plexus epi

57 patients, aggregates were more prominent as nuclear inclusions in NADPH-diaphorase neurons, with les

58 nt is expressed in transgenic mice, it forms nuclear inclusions in neurons and causes early death.

59 similar clinical findings and of viral-like nuclear inclusions in osteoclasts, we hypothesized that

60 4 protein is associated with cytoplasmic and nuclear inclusions in productively infected keratinocyte

61 ology revealed by this reporter and ataxin-7 nuclear inclusions in the vulnerable neurons.

62 Q] in that ataxin-1[82Q]-A776 failed to form nuclear inclusions in tissue culture cells.

63 nd their relocalization into E4-ORF3-induced nuclear inclusions is required for this modification to

64 oxide synthase-positive neurons (which lack nuclear inclusions), loss of nerve fibers in the myenter

65 with an expanded polyglutamine repeat led to nuclear inclusion (NI) formation and late-onset cell deg

66 rounding polyQ specifies the constituents of nuclear inclusions (NI) formed by the disease protein.

67 e 1 (SCA1), aggregates in ubiquitin-positive nuclear inclusions (NI) that alter proteasome distributi

68 lutamine proteins form aggregates, including nuclear inclusions (NI), within neurons, possibly due to

69 generative pathology, and ubiquitin-positive nuclear inclusions (NIs).

70 type-1 (SCA1) and triggers the formation of nuclear inclusions (NIs).

71 seases, the expanded protein aggregates into nuclear inclusions (NIs).

72 Attachment of an exogenous NLS forces nuclear inclusion of Cdc25 in damaged cells.

73 y play a role in various other diseases with nuclear inclusions or foci containing an RNA binding pro

74 opment in the field since the recognition of nuclear inclusions or the propensity of polyglutamine to

75 Neuronal changes in the striatum (nuclear inclusions) preceded the onset of phenotype, whe

76 e observed complexity in the dynamics of the nuclear inclusions provides a molecular explanation for

77 These cells also contain nuclear inclusions, reminiscent of those seen in paramyx

78 ore nucleated than normal and some contained nuclear inclusions similar to those observed in human PD

79 f ATXN7-92Q, inhibiting its aggregation into nuclear inclusions that sequester DUBm components, leadi

80 enic polyQ proteins accumulate in axonal and nuclear inclusions, titrate soluble motor proteins, and

81 pression, mutant ataxin-1, including that in nuclear inclusions, was cleared rapidly from Purkinje ce

82 Nuclear inclusions were present, suggesting that the dis

83 Nuclear inclusions were purified to near homogeneity, an

84 Cs, i.e., the short CTs reveal predominantly nuclear inclusions, whereas the long CTs prominently rev

85 plications in the formation of the insoluble nuclear inclusions, which are characteristic of codon re

86 Intriguingly, the enrichment of nuclear inclusions with slow dynamics parallels changes