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1 se chain reaction (PCR) were used to examine transcriptional dysregulation.
2 containing transcripts but do display global transcriptional dysregulation.
3 letion and unique profiles of DNA damage and transcriptional dysregulation.
4 eting, chromatin disruption, and ultimately, transcriptional dysregulation.
5 tional co-activators resulting in widespread transcriptional dysregulation.
6 cal effect of the expanded protein is due to transcriptional dysregulation.
7 to induce cytoplasmic neurodegeneration and transcriptional dysregulation.
8 rt their effect through a complex pattern of transcriptional dysregulation.
9 a leukemic phenotype through common modes of transcriptional dysregulation.
11 both MSN and nNOS-IN, indicating that global transcriptional dysregulation alone does not account for
13 observe clear progressive, striatal-specific transcriptional dysregulation and accumulation of neuron
14 HSCs lacking miR-29a/b-1 exhibit widespread transcriptional dysregulation and adopt gene expression
16 s in vitro, leading to increased cell death, transcriptional dysregulation and cell-type-specific mol
19 Huntington's disease (HD) is associated with transcriptional dysregulation, and multiple studies with
21 demonstrates that histone deacetylation and transcriptional dysregulation are two early, largely ind
22 2, a NRG3 risk polymorphism, suggesting NRG3 transcriptional dysregulation as a molecular mechanism o
23 , proteins with expanded polyglutamine cause transcriptional dysregulation before onset of symptoms,
25 irradiation, XP-D/CS cells displayed a gross transcriptional dysregulation compared with "pure" XP-D
27 he extensive Huntington's disease-associated transcriptional dysregulation, consistent with treatment
28 hould help elucidate the mechanisms by which transcriptional dysregulation contributes to neuronal dy
30 ration in HD have not been fully elucidated, transcriptional dysregulation has been implicated in dis
37 erapies.Significance: Systematic analysis of transcriptional dysregulation in cancer cell lines and p
39 n (LCM) study to examine the contribution of transcriptional dysregulation in candidate genes involve
40 d inclusions (FTLD-U), suggesting a role for transcriptional dysregulation in FTLD-U pathophysiology.
43 elevant mutation causes synapse deficits and transcriptional dysregulation in human neurons and our f
44 htt to accumulate in the nucleus, leading to transcriptional dysregulation in Huntington disease (HD)
48 d exerts a deleterious effect through remote transcriptional dysregulation in specific progenitor sub
51 basis for, and etiological significance of, transcriptional dysregulation in this context is lacking
53 ex, results in reduced H3K27me3 and profound transcriptional dysregulation, including that of a set o
58 ethylation in Huntington disease (HD), where transcriptional dysregulation is a major factor in patho
62 of polyglutamine toxicity and indicate that transcriptional dysregulation is an important part of th
64 n early component of polyglutamine toxicity, transcriptional dysregulation, is conserved in yeast and
65 als to birth and beyond, despite substantial transcriptional dysregulation, is consistent with mammal
66 trates a distinct disease mechanism by which transcriptional dysregulation leads to an inborn error o
67 e Lange Syndrome, in which global yet subtle transcriptional dysregulation leads to development of at
69 haperones and suggest that context dependent transcriptional dysregulation may contribute to differen
70 utation impairs DNA binding, suggesting that transcriptional dysregulation may contribute to the phen
72 xpression analysis of infected hNPCs reveals transcriptional dysregulation, notably of cell-cycle-rel
73 To determine whether polyglutamine-mediated transcriptional dysregulation occurs in yeast, we expres
74 e multi-omics data revealed that UVR-induced transcriptional dysregulation of a subset of genes was a
78 formation of the majority of lipofuscin and transcriptional dysregulation of genes associated with i
79 pairment through mechanisms dependent on the transcriptional dysregulation of genes required for memo
80 emporal lobe epilepsy (TLE), suggesting that transcriptional dysregulation of HCNs might contribute t
81 k analyses demonstrate prominent MIA-induced transcriptional dysregulation of mTOR and EIF4E-dependen
83 ell line and may represent the major site of transcriptional dysregulation of TGF alpha promoter acti
84 These findings emphasize the importance of transcriptional dysregulation of the autoantigen in auto
85 e hypothalamus, respectively, results in the transcriptional dysregulation of the circadian clock and
86 Since somatic alterations or mutations and transcriptional dysregulation of the FOXO genes are infr
88 ) mice to investigate effects of interneuron transcriptional dysregulation on the dynamics of the I/E
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