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1 ed by large intranuclear protein aggregates (nuclear inclusions).
2 accumulates in a single, ubiquitin-positive nuclear inclusion.
3 XN1 colocalized and interacted with ATXN1 in nuclear inclusions.
4 tion but increase the fraction of cells with nuclear inclusions.
5 g its sequestration away from promoters into nuclear inclusions.
6 omoted the accumulation of mutant ATXN7 into nuclear inclusions.
7 y by the presence of neuropil aggregates and nuclear inclusions.
8 to aggregate and form larger cytoplasmic or 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 th AR species but not to fragment-containing nuclear inclusions.
16 ensity of such cells to form cytoplasmic and nuclear inclusions.
17 ence the appearance or frequency of neuronal nuclear inclusions.
18 ost CBP was not co-localized with huntingtin nuclear inclusions.
19 om the depletion of transcription factors by nuclear inclusions.
20 oduced from the mutant allele is retained in nuclear inclusions.
21 huntingtin, but not normal huntingtin, forms nuclear inclusions.
22 eractive and that contain paramyxovirus-like nuclear inclusions.
23 med vacuoles and filamentous cytoplasmic and nuclear inclusions.
24 that relies on the tobacco etch virus (TEV) nuclear inclusion a (NIa) protease and leads to the coor
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
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
34 BAC-CAG mice show robust striatum-selective nuclear inclusions and transcriptional dysregulation res
35 lation of the mutant Atxn3 protein, abundant nuclear inclusions and, in select brain regions, extranu
36 r membrane blebbing, mitochondrial swelling, nuclear inclusions, and absence of junctional end feet.
38 on and had tubulointerstitial nephritis with nuclear inclusions, apoptosis, and progressive destructi
39 in HD postmortem brains and by the fact that nuclear inclusions are only detected by antibodies to th
40 -glucuronidase (GUS) were placed between the nuclear inclusion b (NIb) and coat protein (CP) domains
41 and that such resistance is counteracted by NUCLEAR INCLUSION B (NIb), the viral RNA-dependent RNA p
42 no acid sequence of the potato virus Y (PVY) nuclear inclusion b protein is highly homologous to the
43 rganize the VICE domain component Hsc70 into nuclear inclusion bodies that resemble VICE domains.
46 a large heterogeneity in the dynamics of the nuclear inclusions compared with the compact and immobil
47 c ganglion cells in PrP-SCA7-92Q mice harbor nuclear inclusions composed of transgene-derived ataxin-
54 ell signaling cascades, is incorporated into nuclear inclusions formed by polyglutamine-containing pr
55 tamine protein, ataxin-3, and establish that nuclear inclusions formed by this protein are aggregates
57 r polyQ tracts led to the formation of intra-nuclear inclusions in a polyQ length-dependent manner du
58 hich aggregate into neuronal cytoplasmic and nuclear inclusions in affected patients, however their c
59 ent of several non-neuronal tissues revealed nuclear inclusions in hepatocytes and choroid plexus epi
60 patients, aggregates were more prominent as nuclear inclusions in NADPH-diaphorase neurons, with les
61 nt is expressed in transgenic mice, it forms nuclear inclusions in neurons and causes early death.
62 similar clinical findings and of viral-like nuclear inclusions in osteoclasts, we hypothesized that
63 4 protein is associated with cytoplasmic and nuclear inclusions in productively infected keratinocyte
66 nd their relocalization into E4-ORF3-induced nuclear inclusions is required for this modification to
67 oxide synthase-positive neurons (which lack nuclear inclusions), loss of nerve fibers in the myenter
68 with an expanded polyglutamine repeat led to nuclear inclusion (NI) formation and late-onset cell deg
70 rounding polyQ specifies the constituents of nuclear inclusions (NI) formed by the disease protein.
71 e 1 (SCA1), aggregates in ubiquitin-positive nuclear inclusions (NI) that alter proteasome distributi
72 lutamine proteins form aggregates, including nuclear inclusions (NI), within neurons, possibly due to
77 mal machinery, facilitating the reduction of nuclear inclusions of both wild-type and mutant huntingt
78 y play a role in various other diseases with nuclear inclusions or foci containing an RNA binding pro
79 opment in the field since the recognition of nuclear inclusions or the propensity of polyglutamine to
81 e observed complexity in the dynamics of the nuclear inclusions provides a molecular explanation for
83 ore nucleated than normal and some contained nuclear inclusions similar to those observed in human PD
84 ar quality control site, a poorly understood nuclear inclusion that coordinates dynamic proteome tria
85 f ATXN7-92Q, inhibiting its aggregation into nuclear inclusions that sequester DUBm components, leadi
86 enic polyQ proteins accumulate in axonal and nuclear inclusions, titrate soluble motor proteins, and
87 pression, mutant ataxin-1, including that in nuclear inclusions, was cleared rapidly from Purkinje ce
90 Cs, i.e., the short CTs reveal predominantly nuclear inclusions, whereas the long CTs prominently rev
91 plications in the formation of the insoluble nuclear inclusions, which are characteristic of codon re