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1 plication within oriP is at or near the dyad symmetry element.
2 contacts to BS12 and E1 contacts to the dyad symmetry element.
3 of repeats, and 4 are found within the dyad symmetry element.
4 ing crystallographically forbidden five-fold symmetry elements.
5 ling the c-axis and removing one-half of the symmetry elements.
6 ry specified by the combination of C4 and C3 symmetry elements.
7 ts adjacent to 3-fold and 5-fold icosahedral symmetry elements and that folding is slower in regions
8 the binding site relative to the icosahedral symmetry elements, and the orientation of the Fab struct
9 only of the spacer and two surrounding 13 bp symmetry elements arranged in inverse orientation; thus,
12 transcription through binding to three dyad-symmetry elements, Box I, Box II and Box III, located in
13 binding of TRF1, TRF2, and hRap1 to the dyad symmetry element but were not essential for the binding
14 activator binding site, disrupting the dyad-symmetry element, caused constitutive, B6 -independent e
16 ides a unified understanding of how specific symmetry elements dictate layer- and state-dependent spi
21 sults, we were able to identify a 26-bp dyad symmetry element immediately upstream of the -35 regions
22 ough a highly convergent route that exploits symmetry elements inherent within this molecule and deli
25 PARP gene in superhelical DNA where the dyad symmetry elements likely form hairpins according to DNas
27 ectively associate to generate the different symmetry elements needed to form higher-order architectu
34 (R,R)-tartaric acid, which destroy existing symmetry elements of the underlying metal and directly b
35 milar to that of the Epstein-Barr virus dyad symmetry element oriP, suggesting a requirement for such
38 al product was quickly accessed using latent symmetry elements, whereby a group-selective, Lewis acid
39 ins the family of repeats but lacks the dyad symmetry element whose replication can be detected for a