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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
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
11 senescence-associated heterochromatic foci (SAHF), containing heterochromatin proteins such as HP1,
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
21 senescence-associated heterochromatic foci (SAHFs), which may provide a chromatin buffer that preven
23 s genomic profile and their implications for SAHF formation and gene regulation during senescence.
26 ins are not required for the accumulation in SAHF of histone H3 methylated on lysine 9, the recruitme
33 pathway cooperates with pRB and p53 to make SAHF, with the HIRA/ASF1a and pRB pathways acting in par
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
42 alization to PML bodies prevent formation of SAHF, as does a PML-RARalpha fusion protein which disrup
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
53 me3-positive heterochromatin, thus promoting SAHF formation, which could be inhibited by ectopic LMNB
61 hese repressive marks remains unchanged upon SAHF formation, suggesting that in somatic cells, hetero
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