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1                                              SAHF contain known heterochromatin-forming proteins, suc
2                                              SAHF formation coincides with the recruitment of heteroc
3                                              SAHF is enriched in a transcription-silencing histone H2
4                                              SAHF represses expression of proliferation-promoting gen
5                                Notably, both SAHF formation and the silencing of E2F target genes dep
6 ration-promoting genes that are repressed by SAHF and associates with histone methyltransferase activ
7 ASF1a drive formation of macroH2A-containing SAHF and senescence-associated cell cycle exit, via a pa
8       Conversely, BRG1 overexpression drives SAHF formation and senescence in a DNA damage-independen
9  senescence-associated heterochromatic foci (SAHF) formation in human fibroblasts.
10  senescence-associated heterochromatic foci (SAHF), and beta-gal staining.
11  senescence-associated heterochromatic foci (SAHF), containing heterochromatin proteins such as HP1,
12  senescence-associated heterochromatic foci (SAHF).
13  senescence-associated heterochromatin foci (SAHF) and cell cycle exit.
14  senescence-associated heterochromatin foci (SAHF), are thought to contribute to the irreversible cel
15  senescence-associated heterochromatin foci (SAHF), as well as specific families of non-genic and gen
16  Senescence-Associated Heterochromatin Foci (SAHF), which are thought to repress expression of prolif
17  senescence-associated heterochromatin foci (SAHF), which repress expression of proliferation-promoti
18  senescence-associated heterochromatin foci (SAHF), which repress expression of proliferation-promoti
19  senescence-associated heterochromatin foci (SAHF).
20  senescence-associated heterochromatin foci (SAHF).
21  senescence-associated heterochromatic foci (SAHFs), which may provide a chromatin buffer that preven
22  senescence-associated heterochromatic foci (SAHFs).
23 s genomic profile and their implications for SAHF formation and gene regulation during senescence.
24       Here we show that BRG1 is required for SAHF formation and senescence induced by oncogenic RAS o
25             How SASP genes are excluded from SAHF-mediated global gene silencing remains unclear.
26 ins are not required for the accumulation in SAHF of histone H3 methylated on lysine 9, the recruitme
27  of histone H3, a site that is methylated in SAHF.
28         Furthermore, BRG1 knockdown inhibits SAHF formation and senescence induced by BRCA1 knockdown
29 tectably affect chromosome condensation into SAHF.
30 for efficient incorporation of HP1gamma into SAHF.
31 es with incorporation of SASP gene loci into SAHF.
32  prior to incorporation of HP1 proteins into SAHF.
33  pathway cooperates with pRB and p53 to make SAHF, with the HIRA/ASF1a and pRB pathways acting in par
34 ated the composition and mode of assembly of SAHF and its contribution to cell cycle exit.
35                 The possible contribution of SAHF to tumor suppression and tissue aging is also criti
36 ence, and ASF1a is required for formation of SAHF and efficient senescence-associated cell cycle exit
37 or, ASF1a, is rate limiting for formation of SAHF and onset of senescence, and ASF1a is required for
38 lization of HIRA to PML bodies, formation of SAHF and senescence, likely through GSK3beta-mediated ph
39   BRG1 knockdown suppresses the formation of SAHF and senescence, while it has no effect on BRCA1 chr
40                                 Formation of SAHF in human cells is driven by a complex of histone ch
41                                 Formation of SAHF is driven by a complex of histone chaperones, HIRA
42 alization to PML bodies prevent formation of SAHF, as does a PML-RARalpha fusion protein which disrup
43       UBN1 is indispensable for formation of SAHF.
44 A to PML bodies is required for formation of SAHF.
45 istone chaperone, ASF1a, drives formation of SAHF.
46 ASF1a), plays a key role in the formation of SAHF.
47 ropose a stepwise model for the formation of SAHF.
48                   Furthermore, modulation of SAHF structure does not affect the occupancy of these re
49 s and are essential structural components of SAHFs.
50 ith both the subsequent layered structure of SAHFs and the global landscape of the repressive marks,
51 h the p16(INK4a) tumor suppressor to promote SAHF formation and proliferative arrest and stabilize se
52 ich BRG1 acts downstream of BRCA1 to promote SAHF formation and senescence.
53 me3-positive heterochromatin, thus promoting SAHF formation, which could be inhibited by ectopic LMNB
54 molecular mechanism by which BRCA1 regulates SAHF formation and senescence is unclear.
55 that each chromosome condenses into a single SAHF focus.
56 P1), and p16(INK4a), but not p53, suppressed SAHF formation induced by BRG1.
57                             However, how the SAHF assembly pathway is activated in senescent cells is
58  essential to identify all components of the SAHF assembly pathway.
59 he structure, assembly and function of these SAHF at a cellular level.
60 cted the series of events that contribute to SAHF formation.
61 hese repressive marks remains unchanged upon SAHF formation, suggesting that in somatic cells, hetero

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