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1 a transcriptionally active site in a BNIP3L enhancer sequence.
2 cts were assayed with a probe containing the enhancer sequence.
3 of multiple nuclear factors with the PTTG 5' enhancer sequence.
4 sfection experiments, we delineated the core enhancer sequence.
5 icing, indicating the presence of a splicing enhancer sequence.
6 associates with a cis-acting recombinational enhancer sequence.
7 ilar to that found in an embryonic stem cell enhancer sequence.
8 t between the silver nanocluster and the DNA enhancer sequence.
9 event PU.1-mediated IRF-4 recruitment to the enhancer sequence.
10 count for the evolutionary invariance of the enhancer sequence.
11 nt of RNA polymerase II complex to the BCAS3 enhancer sequence.
12 operty also constrains this highly conserved enhancer sequence.
13 gene has a hematopoietic-specific functional enhancer sequence.
14 activates splicing through intronic splicing enhancer sequences.
15 nal differences in the mouse and human renin enhancer sequences.
16 rs showed distinct preferences for different enhancer sequences.
17 rus but had acquired various duplications of enhancer sequences.
18 t contain either insulin or albumin promoter/enhancer sequences.
19 splicing from a number of intronic splicing enhancer sequences.
20 which function through binding to the E-box enhancer sequences.
21 l lines and contains negative regulatory and enhancer sequences.
22 ting a position dependence of the U3-encoded enhancer sequences.
23 and DNA recombination via Pax5 and distal 3' enhancer sequences.
24 transcription factor protein binding at the enhancer sequences.
25 issue, suggesting nucleotide polymorphism in enhancer sequences.
26 d CNS depends on both its 5' promoter and 3' enhancer sequences.
27 transgenic mice, using Col2a1 gene promoter/enhancer sequences.
28 identical proximal promoter and far upstream enhancer sequences.
29 cyclic AMP response element (CRE) family of enhancer sequences.
30 at preceded stable association of Prmt5 with enhancer sequences.
31 expression was driven by mouse Pax3 promoter/enhancer sequences.
32 ontaining the promoter and dioxin-responsive enhancer sequences.
33 es that integrate input from multiple distal enhancer sequences.
34 loop between the PPARgamma2 promoter and an enhancer sequence 10 kb upstream that forms at the onset
37 and reporter gene constructs, a 200 bp Grm6 enhancer sequence, a 445 bp Cabp5 promoter sequence, and
38 RNA recognition motif to an exonic splicing enhancer sequence, a phenomenon reversed by SRPK1 phosph
40 ated aryl hydrocarbon receptor to the CYP1A1 enhancer sequence; additionally, NO-aspirin 2 suppressed
41 phenotypes, caused by insertion of the viral enhancer sequences adjacent to an MYB transcription fact
42 f inoculation and the presence of the PyF101 enhancer sequences affected the patterns of MCF generati
43 tion of viral mRNAs containing a translation enhancer sequence also contributes to the disassembly of
46 ted dinucleosome templates using the albumin enhancer sequence and found that site-specific binding o
48 animal regulatory genome and the make-up of enhancer sequences and confirms and generalizes principl
50 intrachromosomal interaction between remote enhancer sequences and the proximal promoter region thro
51 c-Fos and c-Jun bound the cyclin D1 -954 enhancer sequence, and the abundance of c-Fos within thi
52 programmed to take place at tissue-specific enhancer sequences, and our data show that the methylati
56 selective pressures exerted on the EIAV LTR enhancer sequences are different from those exerted on t
57 mink cell focus-inducing (MCF) virus, the U3 enhancer sequences are tandemly repeated in the LTR.
58 viral genome, however, proximally positioned enhancer sequences are unable to confer significant leve
60 eosome positioning properties of the central enhancer sequence assembled into mononucleosome core par
63 wed that E10 splicing involved exon splicing enhancer sequences at the 5' and 3' ends of E10, an exon
64 dent of the activity of known cis-regulatory enhancer sequences at the achaete-scute complex that med
65 to-expression modeling, which interprets the enhancer sequence based on transcription factor concentr
66 and internal deletion constructs shows that enhancer sequences between nucleotides 275 and 329 are i
68 hancers indicates that subtle differences in enhancer sequence can have profound effects on the splic
69 ly, we show that snake and mouse orthologous enhancer sequences can display distinct expression speci
70 subsequent to the addition of the Fis-bound enhancer sequence, catalytic activity was no longer affe
73 ons of zebrafish hoxb3a/hoxb4a promoters and enhancer sequences containing regions of homology that w
74 P3 robustly bind human, but not mouse, GPR15 enhancer sequences, correlating with receptor expression
75 ch included mutants with deletions of exonic enhancer sequences, did not accumulate splicing intermed
77 and identified approximately 6,200 candidate enhancer sequences directly from fetal and adult human h
80 ng human chromosome-21, implicating promoter/enhancer sequence divergence as a factor, including huma
82 of a previously unidentified AAV integration enhancer sequence element which functions in cis to an A
83 IL-1beta gene, while deletion of the kappaB enhancer sequences eliminated BK-stimulated CAT activity
84 -matrix analysis to identify putative exonic enhancer sequences (ESEs), we found multiple high score
87 ing sites are not critical components of the enhancer sequence for PTTG trancriptional activation in
89 members, predominantly c-Rel, interact with enhancer sequences for STAT5, a key transcription factor
90 oxidant response element (ARE), a cis-acting enhancer sequence found in the promoter region of many g
91 ynaptic activity response element (SARE), an enhancer sequence found upstream of many plasticity-rela
94 nambiguously identified three new long-range enhancer sequences functionally in the Nkx2-5 gene in tr
95 TGF-beta and TNF-alpha response elements as enhancer sequences, functioning in the context of a hete
98 Both the epsilony-CACCC site at -114 bp and enhancer sequences (hypersensitive site 2 [HS2]) from th
99 ngs are consistent with the possibility that enhancer sequence hypervariability can alter expression
100 hermodynamics-based models that interpret an enhancer sequence in a given cellular context specified
103 over, LMX1B binds specifically to a putative enhancer sequence in intron 1 of both mouse and human CO
104 Identification of this second functional enhancer sequence in the 5'-promoter region of cathepsin
105 obarbital (PB)-responsive 132-base pair (bp) enhancer sequence in the CYP2B10 gene, we have delimited
107 osine hydroxylase (TH) gene is controlled by enhancer sequences in its 5' flanking region; these enha
112 a profile of protein occupancy in the HTLV-1 enhancer sequences in the presence of high (MT-2) and lo
113 conformations required for interaction with enhancer sequences in the proximal promoter region of th
114 s family of transcription factors within the enhancer sequences in the viral long terminal repeats (L
115 iling, in vivo characterization of candidate enhancer sequences in transgenic mice, and targeted dele
119 e SL3 LTR were tested by inserting the viral enhancer sequences into a plasmid containing the promote
120 ing PCR-amplified, PCR-mutated, or synthetic enhancer sequences into the Ganesh family of P element r
124 forming to this motif, a typical purine-rich enhancer sequence is dispensable for either enhancer act
131 ed for islet-restricted expression: a distal enhancer sequence located between -3 and -6.5 kilobases
133 ivators of sigma54-holoenzyme generally bind enhancer sequences located >70 bp upstream of the promot
134 cularly robust and was refined to a discrete enhancer sequence lying between nt -2832 and -2462 from
136 egion of this gene identified two functional enhancer sequences; namely an Sp1(N)23estrogen-responsiv
138 NGF expression is controlled by promoter and enhancer sequences of a keratin gene, thus restricting t
141 ment has become subject to regulation by eye enhancer sequences of the eya gene, disrupting normal ex
142 W to test the hypothesis that the duplicated enhancer sequences of this virus have a sequence-specifi
143 itutions were introduced into the chimpanzee enhancer sequence or reverted in the human enhancer to t
144 undertaking detailed mutational analyses of enhancer sequences, or those who wish to avoid the diffi
145 ruses is dependent on the duplication of the enhancer sequences present in the unique 3' (U3) region
146 enzymes and antioxidant proteins through an enhancer sequence referred to as the antioxidant-respons
148 ft assays confirm that PAX-FKHR bind to core enhancer sequences showing similarity to consensus PAX3/
150 ed immunoglobulin mu gene is dependent on an enhancer sequence situated within one of the introns of
151 sembles onto the most conserved core of this enhancer sequence specifically in neuronal WERI-1 cell e
152 agents thus far tested is mediated by two 5'-enhancer sequences, SX2 and AB1, but neither fragment wa
153 ate that ESS1 is juxtaposed to a purine-rich enhancer sequence that activates the use of the 5'ss of
155 he SF2/ASF protein to a purine-rich splicing enhancer sequence that is located in the 3' exon of M1 m
156 tions in retinal explants mapped an intronic enhancer sequence that mediated NRL-directed Reep6.1 exp
157 proximal sequences and not on the cis-acting enhancer sequences that bind the aryl hydrocarbon recept
159 ticularly beneficial in the analysis of exon enhancer sequences that function in exon recognition dur
160 udies reported here, we show that additional enhancer sequences that lie outside of the core region a
161 ory specificity of predicted exonic splicing enhancer sequences that may control splicing regulation.
162 about the genomic context of this gene or of enhancer sequences that may direct its diverse functions
163 dentification and characterization of the 3' enhancer sequences that play important roles in this syn
164 t anneal to the exon and contain a 'tail' of enhancer sequences that recruit activating proteins.
165 ified ornithine decarboxylase (ODC) promoter/enhancer sequences that up-regulate target protein expre
167 he intron, and movement of putative intronic enhancer sequences to multiple promoter-proximal sites a
168 ining Myb-binding elements in their promoter/enhancer sequences, to determine whether the phenotypic
170 in craniofacial development and suggest that enhancer sequence variation contributes to the diversity
174 to - 105, encompassing two identical 8-bp DR enhancer sequences, was necessary for CROC-1-mediated tr
175 usage in the clone 9-60 LCL, in which the W enhancer sequences were deleted upstream of Wp1, reveale
176 Cabp5 promoter sequence, and a 164 bp Chx10 enhancer sequence, were defined, each driving reporter e
177 Tf1 integration, suggesting a synergy of Tf1 enhancer sequence with the stress response elements of t
178 anscription of reporter genes containing EPO enhancer sequences with intact, but not mutant, HIF-1 bi
181 We have also identified a G-rich intronic enhancer sequence within the small intron that is essent
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