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1         In the core promoter region both the non-consensus 21 bp spacing and the specific sequence be
2 cing depends on the presence of a suboptimal non-consensus 3' splice site.
3 pothesis that the redundant consensus and/or non-consensus 5' Sp1 binding sites are required to block
4                       The SPO22 intron has a non-consensus 5' splice site (5'SS) that dictates its Na
5 ons causing CTP expression and adoption of a non-consensus 5'-UTR/proximal promoter region.
6              The +1123/+1134 region harbored non-consensus activator protein-1 and Ets1 binding sites
7                       They also suggest that non-consensus alterations in the NKp80 hemITAM, as commo
8 y mutant SF3B1 wherein it is able to utilize non-consensus alternative BP sequences by stabilizing we
9 t the NKp80 hemITAM and demonstrate that two non-consensus amino acids, in particular arginine 6, cri
10 of all major vascular events was similar for non-consensus and classic TIAs (27.1% [95% CI 22.8-31.4]
11 mal expression of aprt , suggesting that the non-consensus and consensus binding sites at the 5' end
12 lps normalize the RPR's rates of cleavage of non-consensus and consensus pre-tRNAs.
13 iting pathogen-specific patterns compared to non-consensus and nonmulti-task clustering approaches.
14 nteractions, particularly when the bases are non-consensus, and that this contributes to setting phys
15                            The presence of a non-consensus androgen response element in the promoter
16 f an overlapping SBE and newly characterized non-consensus AP-1 binding sequence that integrates the
17  exhibits differential activity for distinct non-consensus AP-1 sites present in human papillomavirus
18       We have observed oligosaccharides on a non-consensus asparaginyl residue in the C(H)1 constant
19 consensus base-pair T:A at position 6 or the non-consensus base-pair C:G at position 6.
20                            The occurrence of non-consensus bases within these domains is responsible
21 f1p works through the PED element which is a non-consensus binding site.
22                                              Non-consensus binding sites of transcription factors (TF
23 w that loss of Fyv6 results in activation of non-consensus, branch point (BP) proximal 3' SS transcri
24 ments resulted in the selection of multiple, non-consensus branchpoint sequences.
25 , the first nucleotide binding site contains non-consensus catalytic site residues, including Asp(668
26 e we show that PAP also contains four nearby non-consensus cdk sites that are phosphorylated by MPF.
27           A previous report has identified a non-consensus direct repeat (DR-1) element in the RXRgam
28  of the RXRgamma1 promoter region revealed a non-consensus DR-1 element at -232 bp from the transcrip
29 anscription factor, namely Pdx-1, binds four non-consensus elements in the IGRP promoter.
30 ogenin B1 estrogen responsive unit, with two non-consensus EREs, with higher affinity than one or two
31  motif, and a GATA motif, which overlaps the non-consensus GAS motif.
32 nse element that contains both consensus and non-consensus GAS motifs, two putative Ets binding sites
33 cellosis or Ochrobactrum; (iii) it applies a non-consensus genus concept that disregards taxonomicall
34 rticoid response unit (GRU) comprised of two non-consensus glucocorticoid receptor (GR) binding sites
35 t further understanding of the phenomenon of non-consensus glycosylation can be used to gain fundamen
36  sequence homology comparison indicates that non-consensus glycosylation occurs on Asn residues in th
37 man IgG1 antibody resulted in an increase in non-consensus glycosylation to 3.15%, a greater than 4-f
38 ivity of wild-type R can be modulated by its non-consensus "head" sequence but this modulation became
39 ing the RAG-SE complex, we hypothesized that non-consensus heptamer sequences might affect PCC stabil
40                         We find that certain non-consensus heptamers, including a cryptic heptamer im
41                          Finally, additional non-consensus interactions, mediated by C-degron binding
42               For PCH2, a long 5' exon and a non-consensus intron branchpoint dictate Nam8-dependence
43 -responsive genes, we identified clusters of non-consensus kappaB DNA sites, many exhibiting low affi
44  clusters with greater coherence compared to non-consensus methods.
45  results suggested further definition of the non-consensus motifs, and database searches with these u
46 fects both domestic and wild cats, encodes a non-consensus myristoylation sequence not utilized by it
47 nterestingly, the 577 bp fragment contains a non-consensus nuclear factor kappaB (NF-kappaB)-binding
48 tein makes numerous specific contacts to the non-consensus nucleotides in the loop E motif (S-turn) i
49 , metA and metC, suggests that in vivo, with non-consensus operators, the repressor binds to at least
50 of homology with certain previously reported non-consensus p53 binding sequences.
51     Additional experiments revealed a second non-consensus Pax-6 binding site in the -306/-274 IGRP p
52                           Here we identify a non-consensus PBD binding site within Dbf4 and demonstra
53               The HCDCREL-1 gene possesses a non-consensus polyadenylation signal that apparently is
54 tative information in both the consensus and non-consensus positions.
55  exhibit dramatic transcriptional defects on non-consensus promoters.
56 6 degrees ), but is much less sharp with the non-consensus purine-purine steps A6G7 and G6G7 (roll an
57 een the consensus pyrimidine-purine step and non-consensus purine-purine steps at positions 6-7 both
58 onsensus pyrimidine-purine step T6G7 and the non-consensus pyrimidine-purine step C6G7 (roll angles o
59 that CAP discriminates between consensus and non-consensus pyrimidine-purine steps at positions 6-7 s
60                 These data suggest that some non-consensus RSS, frequently present at chromosomal tra
61  found to bind chromosome tightly, likely at non-consensus sequence sites.
62 interactions were stronger on DNA containing non-consensus sequences, like those of typical promoters
63 ination was highly active on a wide range of non-consensus sequences.
64 licing at multiple sites, some of which have non-consensus sequences.
65  utilization of a 5' splice site at -I and a non-consensus site at +1.
66 Ngamma-activation site (GAS) overlapped by a non-consensus site for nuclear factor kappa B (NFkappaB)
67  address whether E2F1 directly bound to this non-consensus site, we demonstrated that the DNA binding
68 E2F1 and a factor that binds adjacent to the non-consensus site.
69 UMO and BLM are required for modification at non-consensus sites and that preferential SUMO-2/3 modif
70 ensus sites were phosphorylated prior to the non-consensus sites at metaphase of meiosis I, and remai
71 remained so throughout maturation, while the non-consensus sites did not become fully phosphorylated
72                              U1A binds novel non-consensus sites upstream of the secretory poly(A) si
73  10-fold lower concentration of MPF than the non-consensus sites.
74 s of exons spliced in aberrant order were at non-consensus sites.
75 ar DNA oligonucleotides and plasmids at many non-consensus sites.
76 oribosyltransferase (aprt) gene contains one non-consensus Sp1 binding site at its 5' end followed by
77 eve that we have identified a cross-species, non-consensus Sp1-binding site that binds Sp1 and that a
78 urthermore we have identified the usage of a non-consensus splice donor site in four families with an
79 f a yeast protein involved in recognition of non-consensus splice donor sites.
80 HOP2 and SAE3) were rescued by conversion of non-consensus splice sites to the consensus sequence.
81 12, splices a class of pre-mRNA introns with non-consensus splice sites.
82 ecific activation segment phosphorylation at non-consensus substrate sites is proposed that is likely
83 vation segment autophosphorylation sites are non-consensus substrate sites.
84                      In NOBOX, we identify a non-consensus SUMO site, K97, that eliminates NOBOX mono
85 preferred sequences, but allow resolution at non-consensus target sites.
86 sus TATA DNA and complexes between TBP and a non-consensus TATA box were kinetically unstable even at
87 ngle and kinetic stability of complexes on a non-consensus TATA box, making them similar to those on
88 cription, particularly from promoters with a non-consensus TATA box.
89                  We also found that TBP bent non-consensus TATA DNA to a lesser degree than consensus
90 ions resulting in increased utilization of a non-consensus TC TATA element of the HIS3 promoter.
91                                        While non-consensus, this sequence still permits both trans-es
92 -day stroke risk after seeking attention for non-consensus TIA (2.9% [95% CI 1.5-4.3]) was still cons
93 r ischaemic stroke (n=1287), classic TIA, or non-consensus TIA (n=570).
94 osterior circulation were more frequent with non-consensus TIA (OR 2.21, 95% CI 1.59-3.08; p<0.0001).
95  and arterial stenoses were also similar for non-consensus TIA and classic TIA, although stenoses in
96                                Patients with non-consensus TIA are at high early and long-term risk o
97 ke risk from time of the index event after a non-consensus TIA was similar to that after classic TIA
98                       However, patients with non-consensus TIA were less likely to seek medical atten
99  of Health Stroke Score <5), classic TIA, or non-consensus TIA were treated according to secondary pr
100                               Designation of non-consensus TIAs as definite cerebrovascular events wi
101                         We have identified a non-consensus, TRalpha2-specific 5' splice site and cons
102  at any given time, the sequences flanking a non-consensus TRE or even the environment in which the c

 
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