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1                                              RNA pol III activity is unchanged in CycD2(-/-) myocardi
2 RNA (TMER) genes that are transcribed from a RNA pol III type 2-like promoter containing triplicated
3 romoters also show enrichment of alternative RNA pol III transcription termination sequences and are
4           Our results show that all analysed RNA pol III expression cassettes (tRNA, U6, Ad VA1), reg
5                  Induction of TBP, Brf1, and RNA pol III-dependent gene expression is driven by enhan
6 role for SUMOylation in controlling Maf1 and RNA pol III-mediated transcription.
7 Given the emerging roles of SENP1, Maf1, and RNA pol III transcription in oncogenesis, our studies su
8 f1 can inhibit the recruitment of TFIIIB and RNA pol III to immobilized templates.
9 sociation of Brf1 complexes with TFIIIC2 and RNA pol III.
10                         Proper initiation by RNA pol III requires the transcription factor TFIIIB.
11  structure enriched with RNAs transcribed by RNA pol III and RNA binding proteins.
12 at many polytene chromosome sites containing RNA pol III genes.
13 miting or stress conditions are encountered, RNA pol III transcription is rapidly repressed through t
14 pressors and oncogenic proteins and enhanced RNA pol III transcription is essential for cellular tran
15 TA-binding protein or c-Myc display enhanced RNA pol III transcription.
16 her, these results demonstrate that enhanced RNA pol III transcription is essential for anchorage-ind
17                                     However, RNA pol III bound to preinitiation complexes or in elong
18 ression and facilitated recycling in a human RNA pol III in vitro system.
19                          RNA polymerase III (RNA pol III) transcribes structural RNAs involved in RNA
20                This load-induced increase in RNA pol III activity is augmented in Rb-deficient hearts
21 ption factor Brf1 prevented this increase in RNA pol III transcription.
22                    Furthermore, increases in RNA pol III-dependent gene activity and TBP levels could
23  complex with BRF that plays a major role in RNA pol III transcription.
24                                    Increased RNA pol III-dependent transcription, observed in transfo
25 uitment to chromatin, resulting in increased RNA pol III occupancy and tRNA expression in cancers.
26                              Ethanol induces RNA pol III-dependent transcription in both HepG2 cells
27  regulator of the load-induced activation of RNA pol III.
28 ts ability to facilitate the dissociation of RNA pol III from these promoters.
29 nscription factor, TBP, and the induction of RNA pol III-dependent gene activity.
30 demonstrate that the X-mediated induction of RNA pol III-dependent genes and increase in TBP are both
31 t chimeric RNAs transcribed from a number of RNA pol III promoters.
32 ults show that transcriptional regulation of RNA pol III and the coordinate control of ribosomal prot
33 C1 and FASN, but with impaired repression of RNA pol III targets.
34 ssary for rapid Maf1-dependent repression of RNA pol III transcription.
35 suggest that BRCA1 is a general repressor of RNA pol III transcription.
36 his report is the first comparative study of RNA pol III-driven promoters expressing short chimeric t
37  TATA box binding protein (TBP), subunits of RNA pol III-specific transcription factor B, in adult my
38  the ability to inhibit the transcription of RNA pol III targets, reduce lipid biogenesis, and lower
39                     Deletion of Sch9 reduces RNA pol III transcription in a Maf1-dependent manner, ye
40 provide a molecular mechanism for regulating RNA pol III transcription through the coordinate control
41 n is of functional importance for regulating RNA pol III-transcribed genes.
42 s, the roles of these proteins in regulating RNA pol III transcription were examined.
43 ss or reduction in JNK1 expression represses RNA pol III transcription.
44  results support the idea that p53 represses RNA pol III transcription through direct interactions wi
45 rtant new role for SUMOylation in repressing RNA pol III-dependent transcription.
46  BRCA1 inhibits both VAI (tRNA) and U6 snRNA RNA pol III transcription; (2) the AD1 of BRCA1 is respo
47 h overexpression of Brf1 modestly stimulated RNA pol III transcription, expression of a phosphomimic,
48         Although it is well established that RNA pol III-dependent transcription is deregulated in tr
49                   Hence, we hypothesize that RNA pol III may be regulated by BRCA1 via the TFIIB fami
50 NK1 positively regulates TBP expression, the RNA pol III-specific factors, Brf1 and Bdp1, JNK2 negati
51 sion levels can be achieved by inserting the RNA pol III expression cassette into the U3 region of th
52 f TARE-6 proceeded in the orientation of the RNA pol III promoter of the Alu dimer and opposite to th
53                  Decreased expression of the RNA pol III-specific transcription factor Brf1 prevented
54                                 In yeast the RNA pol III transcription machinery bound to tRNA genes
55                  We also identify that these RNA pol III type 2-like promoters are conserved in eukar
56 s defective in its ability to associate with RNA pol III.
57      In contrast, gene delivery systems with RNA pol III-based expression cassettes have not been stu
58 protein, the second largest subunit of yeast RNA pol III.

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