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1 zed a third enzyme, PgdB, as a glucosamine N-deacetylase.
2 e of SIR2 is SIRT1, an NAD-dependent histone deacetylase.
3 and show it to encode a sirtuin-type histone deacetylase.
4 , belonging to the class of NAD(+)-dependent deacetylases.
5 (PROTAC), which efficiently degrades histone deacetylases.
6 proteases, nitrilases, caspases, and histone deacetylases.
7 d were associated with inhibition of histone deacetylases.
8 se C; nor do they inhibit class I/II histone deacetylases.
11 histone acetyl-transferase P300 and histone deacetylase 1 (HDAC1) to circularized HBV DNA (which res
14 letion of ARID1A resulted in loss of histone deacetylase 1 binding, increased histone 4 lysine acetyl
15 cluster promoted the recruitment of histone deacetylase 1 to specific target gene promoters and, thu
16 can also be induced by inhibition of histone deacetylases 1 and 2 (HCAC 1/2), which is one of the kno
18 erest, pharmacological inhibition of histone deacetylase 11 (HDAC11) and suppressor of variegation 3-
21 t bacterial-derived lactate inhibits histone deacetylase 11, causing unchecked HDAC6 activity and inc
22 omplexes containing PRMT5 and either histone deacetylase 2 (HDAC2) or HDAC3, enhanced binding of co-a
23 ng variant in the mouse kidney) with histone deacetylase 2 (HDAC2), as well as the function of the Do
24 d a repressive complex by recruiting histone deacetylase 2 to the SIRT3 promoter, and depletion of SR
25 ion, where it interacts with class I histone deacetylases 2 and 3 (HDAC2 and HDAC3) to regulate chrom
29 ic manipulations, we determined that histone deacetylase 3 (HDAC3) negatively regulates Nr4a2 in the
30 ression through interaction with the histone deacetylase 3 (HDAC3)-nuclear receptor corepressor 1 (NC
31 er assay developed, we find that the histone deacetylase 3 (HDAC3)-selective inhibitor, RGFP966, inhi
34 AR2 diminished its interactions with histone deacetylase 3 and beta-catenin, interfering with Wnt coa
44 e microtubule-associated deacetylase histone deacetylase 6 (HDAC6) via a signaling pathway involving
46 ogramming is dependent on functional HISTONE DEACETYLASE 6 and methyltransferase MET1, and transition
47 F2 inhibition, whereas inhibitors of histone deacetylase 6 block the activation of cellular INF2.
48 DNA methyltransferase inhibitors and histone deacetylase 6 inhibitors (DNMTis and HDAC6is) individual
50 of CAP-KAc-actin-inhibited INF2 with histone deacetylase 6 releases INF2 inhibition, whereas inhibito
51 t SIK1 phosphorylated and stabilized histone deacetylase 7 (HDAC7) protein during cardiac stress, an
54 identified a prominent role of HDAC (histone deacetylase)-9 in atherosclerosis and its clinical compl
55 R-335 is epigenetically regulated by histone deacetylases; a screen for suitable histone deacetylase
57 ted expression of an esterase, arylacetamide deacetylase (AADAC), in vascular smooth muscle cells (VS
59 owever, point mutations in the NCoR and SMRT deacetylase-activating domains, which are required for H
60 ut how the multi-subunit complexes influence deacetylase activities and site-selectivities in chromat
61 a SIRT6 variant, R65A, that maintains basal deacetylase activity but cannot be activated and failed
62 mpared with acetylated counterparts, but the deacetylase activity can be stimulated by fatty acids an
64 wn and NMR experiments, we show that HDAC1/2 deacetylase activity in one of the most ancient and evol
65 is primarily a cytoplasmic protein, and its deacetylase activity is focused mainly on nonhistone sub
68 ave been shown to increase the weak in vitro deacetylase activity of SIRT6 but this effect is modest
70 tail is responsible for a sharp reduction in deacetylase activity of the CoREST complex for H3K14ac.
71 multidomain cytosolic enzyme having tubulin deacetylase activity that has been unequivocally assigne
72 and in vivo experiments showed that CobB(L) deacetylase activity was negatively affected when YiaC a
73 kably higher desuccinylase activity, but not deacetylase activity, in proliferative cultured muscle a
74 ers were a result of direct effects of Hdac3 deacetylase activity, we used an HDAC3 selective inhibit
80 icient two-enzyme system, involving a GalNAc deacetylase and a galactosaminidase, for A conversion.
83 tylase (NuRD) complex uniquely combines both deacetylase and remodeling enzymatic activities in a sin
84 ed tetramers prepared using different chitin deacetylases and observed significant differences in pri
85 and kinases) and functionally (e.g., histone deacetylases and proteasome) connected to many validated
86 target associations involving HDACs (histone deacetylases) and sigma receptors by employing modern ap
87 52 repressed PuHDA9, which encodes a histone deacetylase, and led to an increase in acetylation and p
91 ruption of cytoskeletal proteins via histone deacetylases, and the recently discovered DNA damage-ind
92 ) through the activity of enzymes known as N-deacetylases, and this N-deacetylation modulates host-pa
94 de N-deacetylases; however, which of these N-deacetylases are involved in peptidoglycan N-deacetylati
98 produced by three recombinant fungal chitin deacetylases (CDAs) originating from different species,
100 e small-molecule inhibitor targeting histone deacetylase class I, is currently in clinical evaluation
101 heterochromatin by outcompeting the histone deacetylase, Clr3 from sites of heterochromatin formatio
102 teractions link Cdk9, H2Bub1 and the histone deacetylase Clr6-CII, while combined Cdk9 inhibition and
103 t with the known control of the Set3 histone deacetylase complex (HDAC) by H3K4 di-methylation, histo
106 Saccharomyces cerevisiae, a prion form of a deacetylase complex assembles over subtelomeric domains
107 ncovers a previously uncharacterized histone deacetylase complex in plant immunity and highlights the
108 C-Cdk8, together with the Ume6-Rpd3 histone deacetylase complex, represses the essential autophagy g
115 on prodrugs with known inhibitors of histone deacetylase, cyclooxygenase, and pyruvate dehydrogenase
117 three distinct epi-drugs that target histone deacetylase, DNA methylation and bromodomain proteins.
119 tween the microtubule-binding domain and the deacetylase domain was critical for recognition and effi
121 lated FUS, whereas both sirtuins and histone deacetylases families of lysine deacetylases contributed
122 IRT2), a member of the NAD-dependent protein deacetylase family, is involved in type I IFN signaling.
123 1, which play a vital role in regulating the deacetylase function of the enzyme and which are absent
125 y we investigated how the absence of histone deacetylase HDA-2 in the Trichoderma atroviride strain D
126 c interaction between kin-29 and the histone deacetylase hda-4 coupled with subcellular localization
127 auxin/indole-3-acetic acid (AUX/IAA)-histone deacetylase (HDA) and (2) auxin response factor (ARF)-hi
128 auxin/indole-3-acetic acid (AUX/IAA)-histone deacetylase (HDA) and (2) auxin response factor (ARF)-hi
129 acetylase1 (RPD3/HDA1) type class II histone deacetylase HDA15 in Arabidopsis (Arabidopsis thaliana).
130 re and putative elements of the BRAF-histone deacetylase (HDAC) (BHC) chromatin-remodeling complex (L
131 with VPA-mediated inhibition of the histone deacetylase (HDAC) and glycogen synthase kinase-3 (GSK-3
132 study, a series of novel dual-target histone deacetylase (HDAC) and mammalian target of rapamycin (mT
135 he critical period of plasticity via histone deacetylase (HDAC) inhibition, caused adult stress to pr
136 and consistently modulated following histone deacetylase (HDAC) inhibition; three (H1F0, IRGM, and WI
138 report that a small-molecule Class 1 histone deacetylase (HDAC) inhibitor Entinostat (MS-275) enhance
141 ase (DNMT) inhibitor hydralazine and histone deacetylase (HDAC) inhibitor valproic acid (VPA) will re
143 we found that trichostatin A, a pan-histone deacetylase (HDAC) inhibitor, blocked all high glucose-i
144 umor cells are more sensitive to the histone deacetylase (HDAC) inhibitor-induced loss of stemness th
146 rinostat) and selective (romidepsin) histone deacetylase (HDAC) inhibitors elicited metabolic reprogr
148 th Ac(5)Neu5Ac combined with various histone deacetylase (HDAC) inhibitors, including vorinostat, enh
149 ety by restoring hippocampal class I histone deacetylase (HDAC) levels and activity, specifically HDA
150 odomain and extra-terminal (BET) and histone deacetylase (HDAC), potentially serving as promising the
152 tanding the roles of various histone/protein deacetylases (HDAC) are key to promoting Treg-based immu
153 harmacological modulation of class I histone deacetylases (HDAC) has been evaluated as a therapeutic
154 which bound to the promoters of the histone deacetylases HDAC1 and HDAC3 and induced HDAC1 and HDAC3
156 nal KER domain to associate with the histone deacetylases HDAC1/2 and the histone demethylase LSD1, e
158 lysine-specific demethylase Lsd1 and histone deacetylase Hdac2, resulting in the simultaneous removal
159 MutSbeta (Msh2-Msh3 complex) and the histone deacetylase HDAC3 function in the same pathway to drive
162 us studies examining the role of the histone deacetylase Hdac3 within myeloid cells demonstrated that
166 vely regulated by the microtubule-associated deacetylase HDAC6, which functions as a regeneration inh
167 ly significantly modulated protein levels of deacetylase (HDAC8), but also significantly caused dynam
168 I enhanced the activities of Class I histone deacetylases (HDACs 1/2), thereby decreased histone acet
169 egulators physically associated with histone deacetylases (HDACs) and many known players in ASD etiol
176 -42 is an orally active inhibitor of histone deacetylases (HDACs) in clinical trials for multiple mye
180 3/NuRD complex and the activities of histone deacetylases (HDACs), and Tet2 hydroxylase play a critic
181 f lymphomas, including inhibitors of histone deacetylases (HDACs), DNA methyltransferases (DNMTs), en
183 istone acetyltransferases (HATs) and histone deacetylases (HDACs), is necessary for appropriate gene
184 t in PTSD, by (1) altering class IIa histone deacetylases (HDACs), which integrate effects of stress
190 ion by inhibiting the microtubule-associated deacetylase histone deacetylase 6 (HDAC6) via a signalin
191 is showed that 12 genes potentially encode N-deacetylases; however, which of these N-deacetylases are
192 ph), which signals the recruitment of lysine deacetylase Hst2 and the removal of lysine 16 acetylatio
193 have elucidated a role for the Sir2 histone deacetylase in establishing the normal distribution of M
194 monstrate a role for a mitochondrial protein deacetylase in hippocampal neurons in behavioral and GAB
197 otential role of multiple families of lysine deacetylases in the post-translational regulation of DVL
198 al development, but the functions of histone deacetylases in this context are poorly understood.
199 crucial role of HDAC6, a cytoplasmic histone deacetylase, in driving RMS tumor growth, self-renewal,
200 le of Sirtuin 1 (SIRT1), an NAD(+) dependant deacetylase, in improved insulin sensitivity and glucose
201 res, while SIRT6 inhibition using shRNA or a deacetylase-inactive mutant (SIRT6(H133Y)) shortened hum
203 ctivator and repressor, with a non-canonical deacetylase-independent function that is vital for the i
205 roach, we have discovered that rapid histone deacetylase inhibition disrupts super enhancer function
207 We now show that the FDA-approved histone deacetylase inhibitor (HDACi) valproic acid (VPA) correc
208 uton's tyrosine kinase inhibitor and histone deacetylase inhibitor abrogated refractory B-1b cell imm
209 ith this finding, treatment with the histone deacetylase inhibitor givinostat caused a significant in
210 armaceutical residues in water, is a histone deacetylase inhibitor in mammals, and is reported to low
212 udied the effect of the FDA-approved histone deacetylase inhibitor suberanilohydroxamic acid (SAHA).
215 treatment with trichostatin A, a pan-histone deacetylase inhibitor that renders chromatin decondensat
218 ed to investigate the effects of the histone deacetylase inhibitor valproate and all-trans retinoic a
220 e ART-only (control) or ART plus the histone deacetylase inhibitor vorinostat (the kick) and replicat
221 performed two phase I trials of the histone deacetylase inhibitor vorinostat combined with either th
222 be re-activated with Trichostatin A (histone deacetylase inhibitor) and/or 5-aza-dC (an inhibitor of
223 both calcitriol and trichostatin A (histone deacetylase inhibitor), the level of IL-9 reached to the
224 nsisting of sodium butyrate (a broad histone deacetylase inhibitor), UNC0646 (a histone methyltransfe
227 the well-established synergy between histone deacetylase inhibitors (HDACi) and alkylating agents, we
228 ide hydroxamic acid (vorinostat) are histone deacetylase inhibitors (HDACi) approved by the US Food a
232 has been on a class of drugs called histone deacetylase inhibitors (HDACi), which have the potential
237 pharmacological activity.IMPORTANCE Histone deacetylase inhibitors are widely studied HIV latency-re
238 ies cell types that are sensitive to histone deacetylase inhibitors based on their metabolic state, a
240 deacetylases; a screen for suitable histone deacetylase inhibitors identified belinostat as a candid
243 with other epigenetic drugs, such as histone deacetylase inhibitors or differentiation inducers (eg,
244 r amplified by DNA demethylation and histone deacetylase inhibitors providing an exquisite therapeuti
245 In particular, our results with histone deacetylase inhibitors support the view that chromatin a
246 s low-dose DNA methyltransferase and histone deacetylase inhibitors, 5-azacytidine and entinostat, di
252 We have discovered that this mitochondrial deacetylase is specifically upregulated in a context-dep
256 alt-inducible kinase 1 (SIK1) stabilized the deacetylase, leading to increased expression of c-Myc, w
257 P-3-O-((R)-3-hydroxymyristoyl)-N-glucosamine deacetylase (LpxC) is as an attractive target for the di
259 xoO and MXAN_3263/ExoP) and a polysaccharide deacetylase (MXAN_3259/ExoL) are important for formation
260 also correlated with enhanced HDAC4 (histone deacetylase) nuclear export, creating a microdomain for
261 and components of nucleosome remodeling and deacetylase (NuRD) are part of the nuclear PERIOD comple
263 tuin 6 (SIRT6) is a nuclear NAD(+)-dependent deacetylase of histone H3 that regulates genome stabilit
267 Mechanistically, SIRT2, an NAD+-dependent deacetylase, protected neurons from cisplatin cytotoxici
271 termined that the acetyltransferase NuA4 and deacetylase Rpd3 are primarily responsible for the dynam
274 utrient/energy sensor mTOR, NAD(+)-dependent deacetylase SIRT1, hypoxia-inducible factor HIF1alpha, o
276 daptations require the mitochondrial protein deacetylase SIRT3 as they are abolished in SIRT3-deficie
277 DLBCLs are dependent on mitochondrial lysine deacetylase SIRT3 for proliferation, survival, self-rene
280 demonstrated that the NAD-dependent protein deacetylase, SIRT7, and the FOXO4 transcription factor a
282 itors of a target biomolecule, NAD-dependent deacetylase Sirtuin 1, were identified by a contest-base
283 pigenetic modulators, NAD+ dependent histone deacetylase Sirtuin 2 (SIRT2), which upon infection tran
284 transcriptional repression of mitochondrial deacetylase sirtuin 3 (SIRT3) by androgen receptor (AR)
288 ect on the enzymatic activity of the histone deacetylase sirtuin family (SIRT1, SIRT2, SIRT3, SIRT5 a
290 fasting intervals, increasing NAD-dependent deacetylase sirtuin-1 signaling important for glucose an
291 a (DLBCL) significantly induce mitochondrial deacetylase sirtuin-3 (SIRT3) activity, disrupted mitoch
293 ase sirtuin-1 (SIRT1) is a class III histone deacetylase that positively regulates cancer-related pat
294 f histone deactelyase 6 (HDAC6), a cytosolic deacetylase that regulates tubulin acetylation, in CF mi
296 ng on GlcNAc residues, differing from MurNAc deacetylases that lack the metal-coordinating Asp residu
297 as coupled to a switch from type IIa histone deacetylase to p300 histone acetylase binding that corre
299 otein complexes that recruit class I histone deacetylases to the genome to regulate gene expression.