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1 fs for interacting with and activating three lysine acetyltransferases.
2 the nucleus in human cell lines and binds to lysine acetyltransferase 2A (KAT2A, also known as GCN5)
5 increased H3K9Ac through recruitment of the lysine acetyltransferase 2B (KAT2B) and WD repeat-contai
8 MOZ, MORF, and HBO1, which are also known as lysine acetyltransferase 6A (KAT6A), KAT6B, and KAT7, re
9 heterozygous truncating mutations in KAT6B (lysine acetyltransferase 6B, formerly known as MYST4 and
10 t-chain family member 2 (ACSS2) coupled with lysine acetyltransferase 7 (KAT7) modulates beta-hydroxy
13 and long-lasting) activation of two distinct lysine acetyltransferase activities along with the ERK/M
15 estigated short- and long-term regulation of lysine acetyltransferase activity and the ERK/mitogen-ac
16 P-ZNF384 fusions resulted in loss of histone lysine acetyltransferase activity in a dominant-negative
17 usal relationship between ERK activation and lysine acetyltransferase activity in insular cortex.
18 ence that these TFs, in conjunction with the lysine acetyltransferase activity of p300/CBP, facilitat
21 selective small molecule inhibitors of their lysine acetyltransferase activity, we validate CBP/p300
24 ules, therapeutics targeting the activity of lysine acetyltransferases and lysine deacetylase enzymes
35 paralogous transcriptional coactivators and lysine acetyltransferases CREB binding protein (CBP) and
36 ng 21 (TRIM21), which activates CREB binding lysine acetyltransferase (CREBBP) via its E3 ligase acti
37 n events is indicated by the associations of lysine acetyltransferases, deacetylases, and acetyl-lysi
38 ntrast the role of missense mutations in the lysine acetyltransferase domain that are more frequently
40 le substrates for the cAMP-dependent protein lysine acetyltransferase from Mycobacterium tuberculosis
41 is implicated in neurodegeneration, and the lysine acetyltransferase GCN5 (also known as KAT2A) is i
42 ucleosome remodelers INO80 or ISW1A, and the lysine acetyltransferases Gcn5 and Esa1 each contribute
45 that pharmacological inhibition of KAT2B, a lysine acetyltransferase identified by our genetic scree
46 fied Gcn5 as the first transcription-related lysine acetyltransferase in 1996, providing a molecular
47 anism of FadD33 by the mycobacterial protein lysine acetyltransferase in a cAMP-dependent manner.
50 comprise the KAT3 family of histone/protein lysine acetyltransferases, interact with over 50 T-lymph
51 and the consequences of loss of SAGA complex lysine acetyltransferase (KAT) activity on histone acety
55 , reversible binding of the inhibitor to the lysine acetyltransferase (KAT) domain of p300 is largely
56 Here, we explore an emerging concept that lysine acetyltransferase (KAT) enzymes drive cellular pl
59 nal lysine acetylation and the corresponding lysine acetyltransferase (KAT) in RC nucleosome assembly
62 we focused on ADA2B, the only subunit in the lysine acetyltransferase (KAT) module that specifically
63 t ID approach, we identified the coactivator lysine acetyltransferase (KAT) p300 as a key IRF4 partne
67 ing clinically targeted, the role of histone lysine acetyltransferases (KAT) in malignancy is less we
68 characterize cellular functions of the human lysine acetyltransferases KAT2A (GCN5) and KAT2B (PCAF),
70 ydroxynaphthoquinone-based inhibitors of the lysine acetyltransferase KAT3B (p300), such as plumbagin
73 4 nucleosome-binding domains and activates 3 lysine acetyltransferases (KAT6A, KAT6B, and KAT7), sugg
74 Mis18 complex is to transiently recruit the lysine acetyltransferase KAT7 to centromeres to facilita
76 n acetylation and deacetylation catalysed by lysine acetyltransferases (KATs) and deacetylases (KDACs
77 r proteins that is catalysed by the 'writer' lysine acetyltransferases (KATs) and mediates interactio
82 ctivation of EP300/CREBB paralogous cellular lysine acetyltransferases (KATs) during the early phase
84 ogical and pathological functions of protein lysine acetyltransferases (KATs) greatly depends on the
88 P/KAT3A) and its paralogue EP300 (KAT3B) are lysine acetyltransferases (KATs) that are essential for
93 acetylation, which is regulated by either a lysine acetyltransferase or a lysine deacetylase enzyme.
94 oyl-CoA, function as efficient substrates of lysine acetyltransferase p300 and serve as sensitive rea
95 tilizes bifunctional molecules to direct the lysine acetyltransferase p300/CBP to proteins fused with
96 following acute inhibition of major cellular lysine acetyltransferases P300 and CBP in hematological
98 ltransferases G9a, GLP and SETD7 and histone lysine acetyltransferases PCAF and GCN5 do somewhat tole
99 g highlights an expanded landscape of orphan lysine acetyltransferases present in the human genome an
105 regulate the lysine acetylation of a 42 kDa lysine acetyltransferase substrate, suggesting a causal
110 AT6A and KAT6B genes are two closely related lysine acetyltransferases that transfer an acetyl group
112 activating phase of the circadian cycle, the lysine acetyltransferase TIP60 acetylates the transcript