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1 ltransferase tat-interactive protein 60 kDa (Tip60).
2 es degradation-independent ubiquitination of TIP60.
3 and this is partly due to destabilization of Tip60.
4 dependent apoptotic pathway by destabilizing Tip60.
5 expression of GRIP1 synergizes the action of Tip60.
6 reases the ability of ATXN1 to interact with Tip60.
7 n methylation and acetylation of p53 through Tip60.
8 methylase LSD1 and histone acetyltransferase Tip60.
9 ir via HRR; effectively phenocopying loss of TIP60.
10 iator and a p53 activator, is a regulator of Tip60.
11 through the action of the acetyltransferase Tip60.
12 promoting USP7-mediated deubiquitination of Tip60.
13 -mediated p53 and lysine acetyl transferase, Tip60.
14 mimic" GK-X-GK motif that is diacetylated by Tip60.
16 We show that the lysine acetyltransferase Tip60 acetylates eEF1A1, whereas the histone deacetylase
18 ircadian cycle, the lysine acetyltransferase TIP60 acetylates the transcriptional activator BMAL1 lea
19 PARP activities mechanistically by directing Tip60 acetylation of histone H2A lysine 5 at the 5' end
20 atory posttranslational modifications impact TIP60 acetyltransferase activity to influence the outcom
22 and that the interaction is dependent on the TIP60 acetyltransferase domain and c-Myb transactivation
24 mbers of the MYST (MOZ, Ybf2/Sas3, Sas2, and TIP60) acetyltransferase family, hMOF and TIP60, are SIR
25 at the HIV-1 Tat-interacting protein 60 kDa (Tip60) acetyltransferase mediates acetylation at lysine
27 ce the degradation of Tip60, suggesting that Tip60 action may not be required for activation of the A
29 ur studies demonstrate that STAT-5 regulates Tip60 activation and this occurs in part by targeting gl
33 hin a distinct complex that presumably lacks TIP60 and appears to be involved in the transcriptional
35 he histone acetyltransferase (HAT) domain of TIP60 and blocks both its enzymatic activity and its coa
36 oplasticity genes show reduced enrichment of Tip60 and epigentic acetylation signatures at all gene l
38 A minimum FOXP3 ensemble containing native TIP60 and HDAC7 is necessary for IL-2 production regulat
39 ificantly decreased the association of KLF4, Tip60 and HDAC7 with HDC promoter, suggesting that gastr
41 as a scaffolding protein for both Dnmt1 and Tip60 and is required for Tip60-mediated acetylation of
42 inal activation domain associates with TRRAP/TIP60 and mixed-lineage-leukemia (MLL1/MLL2) SET1-type c
43 ntified SIRT1 that specifically deacetylates TIP60 and negatively regulates TIP60 activity in vivo.
44 ation, we found that the interaction between TIP60 and p53 is severely inhibited in the presence of U
49 at UHRF1 is a critical negative regulator of TIP60 and suggest that UHRF1-mediated effects on p53 may
50 NA-associated AGO2 interacted with MMSET and Tip60 and that the diRNA binding and catalytic activitie
51 d potential regulatory relationships between TIP60 and the c-Myb oncoprotein in hematopoietic cells.
52 exes control access of factors such as E2F1, Tip60, and HDAC1/2/3 to the promoters of various cell-cy
53 sttranslational modifications involving p38, Tip60, and PRAK, three proteins that are essential for r
61 n, we showed the co-occupancy of ERbeta1 and Tip60 at ERE and AP-1 sites of ERbeta1 target genes.
68 HD and RING finger domains 1) interacts with TIP60 both in vitro and in vivo and induces degradation-
71 ing activities and repair factors, including Tip60, BRG1 and NBS1, and renders mice hypersensitive to
77 zing cycloheximide treatment, we showed that TIP60 catalytic activity is required for stabilization o
78 d this phenomenon further and found that the TIP60 chromatin-regulatory complex is essential for Nrf1
80 for the lysine acetyltransferase activity of TIP60.com but not for that of the pure recombinant TIP60
86 g enzyme, exists as an integral subunit of a TIP60 complex but also resides within a distinct complex
88 activity of Tip60/NuA4, implicating the Rvb1-Tip60 complex in the chromatin-remodeling response of ce
90 ort a model in which NPAT recruits the TRRAP-Tip60 complex to histone gene promoters to coordinate th
91 r an intricate mechanism orchestrated by the TIP60 complex to regulate 53BP1-dependent repair through
92 ns MLL-like complex cooperates with the NuA4/TIP60 complex to regulate the expression of a novel effe
93 ting acetylation of the H4 tail (by the NuA4-Tip60 complex) and shifting the chromatin to a more open
94 tone acetyltransferase (HAT) activity of the Tip60 complex, and histone H4 acetylation is required pr
95 ein (TRRAP) and Tip60, two components of the Tip60 complex, associate with histone gene promoters at
96 d with mutations in the Trrap subunit of the TIP60 complex, both in the cell line panel and in a huma
97 orrelation with the association of the TRRAP-Tip60 complex, histone H4 acetylation at histone gene pr
101 hromatin remodeling SRCAP, hINO80, and TRRAP/TIP60 complexes, and the nutrient sensing complex Uri/Pr
103 the histone acetyltransferase complex, NuA4/TIP60, cooperates with the C. elegans MLL-like complex i
106 findings reveal that phosphorylation directs TIP60-dependent acetylation to promote homologous recomb
108 thway, which is preliminarily activated by a Tip60-dependent mechanism in response to chromatin relax
109 hylation at position R205, which facilitates TIP60-dependent mobilization of 53BP1 from DNA breaks, p
111 protein that binds H4K12ac, phenocopies the Tip60 depletion with respect to heterochromatin decompac
117 anisms that include the direct inhibition of TIP60 enzymatic activity described here and the previous
120 mediated by APP and that, remarkably, excess Tip60 exerts a neuroprotective role in APP-induced axona
121 ckdown of ATF3 expression leads to decreased Tip60 expression and suppression of ATM signalling as ev
128 1), a member of the MYST (Moz-Ybf2/Sas3-Sas2-Tip60) family of histone acetyltransferases (HATs), is t
130 erminal 106-190 aa of FOXP3 are required for TIP60-FOXP3, HDAC7-FOXP3 association, as well as for the
135 a novel functional interactive role between Tip60 HAT activity and APP in axonal transport and provi
138 ing genetic approaches, we show that loss of Tip60 HAT activity in the presence of the Alzheimer's di
141 onents of the SRCAP chromatin remodeling and TIP60 HAT complexes, whereas the small complex possesses
142 n and weakened rhythmicity, whereas reducing Tip60 HAT expression drastically weakened rhythmicity.
146 t partly by decreasing the formation of KLF4/Tip60/HDAC7 repressive complexes at the HDC promoter.
148 w that NPAT interacts with components of the Tip60 histone acetyltransferase complex through a novel
152 ontin functions as a platform for recruiting Tip60 histone acetyltransferase with increased H4 acetyl
155 IPPED-A protein, a scaffold for the SAGA and Tip60 histone modifying complexes, interacts with GFP-CL
160 s supported by the finding that depletion of Tip60 in Fanconi anemia cells does not increase sensitiv
162 ctivity is required for the stabilization of Tip60 in order to operate an effective p53-dependent apo
165 through phosphorylation of Thr158; activated Tip60 in turn directly interacts with and induces the pr
166 More importantly, depletion of RUVBL1 or TIP60 in various cancer cells sensitized them to cell de
167 Moreover, Ran was acetylated by CBP/p300 and Tip60 in vitro and on transferase overexpression in vivo
170 rotein acetyltransferase KAT5 (also known as TIP60) increases after DNA damage in a manner that promo
171 tomycin C in normal fibroblasts depleted for Tip60 indicates a direct function in interstrand cross-l
172 ylation of the enzymatic domains of hMOF and TIP60 inhibits their acetyltransferase activity and prom
173 HPV E6 also relieves cellular promoters from TIP60-initiated repression and abrogates p53-dependent a
176 roach, the biological relevance of the ATXN1/Tip60 interaction was assessed by crossing ATXN1[82Q] mi
177 find that the chromatin remodeling protein, Tip60, interacts directly with the FANCD2 protein in a y
178 rther show that AICD, together with Fe65 and Tip60, interacts with the LRP1 promoter and suppresses i
185 oietic cells, leading us to hypothesize that TIP60 is a normal regulator of c-Myb function and that d
189 is defective, the histone acetyltransferase Tip60 is recruited to pericentric heterochromatin, where
191 The acetylation of ATM on lysine 3016 by Tip60 is therefore a key step linking the detection of D
192 DNA damage, the binding of SIRT1 to hMOF and TIP60 is transiently interrupted, with corresponding hMO
196 rase MMSET (WHSC1) and the acetyltransferase Tip60 (KAT5) to the DSB, where local levels of histone H
199 HP10 colocalize to nuclear foci positive for TIP60, known to activate ATM at sites of DNA damage.
200 by reduced locomotion activity of the mutant Tip60 larvae, and these phenotypes can be partially resc
201 Furthermore, in such a context, depletion of Tip60 leads to derepression of satellite transcription,
205 yb function and that dysregulated or mutated TIP60 may contribute to c-Myb-driven leukemogenesis.
206 together, our findings provide evidence that TIP60 may contribute to SCC progression by increasing De
207 Our findings reveal a novel mechanism for Tip60 mediated sleep-wake regulation via control of axon
208 for both Dnmt1 and Tip60 and is required for Tip60-mediated acetylation of Dnmt1 and subsequent Dnmt1
211 uced cellular transformation by facilitating Tip60-mediated degradation of Dmnt1 and promoting apopto
214 ce of UHRF1, suggesting that UHRF1 modulates TIP60-mediated functions in both K120 acetylation-depend
215 ied a BRD-reader function of PCAF that bound TIP60-mediated histone acetylations at DSBs to recruit a
219 or abolish the ability of the resulting NuA4/TIP60 multi-subunit complexes to acetylate the histone H
220 , following DNA damage the acetyltransferase Tip60 must acetylate ATM proteins prior to their full ac
221 inger (MOZ)/KAT6A is a MOZ, Ybf2/Sas3, Sas2, Tip60 (MYST)-type histone acetyltransferase that functio
222 In summary, these studies demonstrate that TIP60 negatively modulates c-Myb transcriptional activit
223 dy provides a framework for manipulating the TIP60-Nrf1 axis to alter proteasome function in various
224 2-related CBP activator protein (SRCAP), and Tip60/NuA4 complexes, but their molecular function is un
225 e of Rvb1 in maintaining the HAT activity of Tip60/NuA4, implicating the Rvb1-Tip60 complex in the ch
227 autoacetylation leads to the dissociation of TIP60 oligomer and enhances its interaction with substra
229 his study, we report that phosphorylation of TIP60 on serines 90 and 86 is important for limiting the
234 MT1-associated protein 1) is a member of the TIP60-p400 complex that maintains embryonic stem (ES) ce
235 e phenotypes of loss of other members of the TIP60-p400 complex, Dmap1(-/-) mice died during preimpla
238 ociated protein 1 (DMAP1) is a member of the TIP60-p400 histone acetyl transferase (HAT) complex, whi
244 antation epigenetic reprogramming processes: TIP60-p400 nucleosome remodeling and DNMT1 maintenance m
245 Hdac6 is necessary for regulation of most Tip60-p400 target genes, particularly those repressed by
246 ly, we find that, like canonical subunits of Tip60-p400, Hdac6 is necessary for robust ESC differenti
250 te that a multifunctional acetyltransferase, Tip60, plays an essential role in oncogenic ras-induced
254 quired for the acetyltransferase activity of TIP60, promoting histone H4K16 acetylation, which facili
255 gether, our results support a model by which Tip60 protects against neurological impairments in diffe
256 n of ATF2 expression in these lines restored TIP60 protein levels and both basal and IR-induced level
258 t with these observations, Nrf1, RUVBL1, and TIP60 proteins were co-recruited to the promoter regions
260 nt promotes, whereas knockdown of endogenous TIP60 relieved, FOXP3-mediated transcriptional repressio
261 (PP2A)B subunit, Tat-interactive protein 60 (TIP60), replication protein A1 (RPA1), and RPA2 proteins
262 ations in SIRT1-targeted lysines on hMOF and TIP60 repress DNA double-strand break repair and inhibit
267 er, the ATF3-Tip60 interaction increases the Tip60 stability by promoting USP7-mediated deubiquitinat
270 howed that HDAC7 was pulled down by KLF4 and Tip60, suggesting that these three proteins form a repre
271 have been shown to induce the degradation of Tip60, suggesting that Tip60 action may not be required
273 concomitant epigenetic repression of common Tip60 target neuroplasticity genes occurs early in multi
275 plex that includes histone acetyltransferase TIP60 (Tat-interactive protein, 60 kDa) and class II his
276 alian pericentric heterochromatin relying on Tip60 that might be dependent on BRD2 recruitment by H4K
277 interact with the histone acetyltransferase Tip60, the histone deacetylase HDAC7, and the Ikaros fam
282 ically interacts with and regulates hMOF and TIP60 through deacetylation and provide additional mecha
283 38 induces the acetyltransferase activity of Tip60 through phosphorylation of Thr158; activated Tip60
285 e reader domain for H4K20me1/2, MBTD1 allows TIP60 to associate with specific gene promoters and to p
289 break repair and inhibit the ability of hMOF/TIP60 to induce apoptosis in response to DNA double-stra
290 red for the binding of the acetyltransferase Tip60 to p53 and for the subsequent acetylation of p53.
292 vation domain-associated protein (TRRAP) and Tip60, two components of the Tip60 complex, associate wi
296 ation at lysine 165 by the acetyltransferase Tip60, which is a prerequisite for its phosphorylation,
297 lysine acetyltransferase, previously called TIP60, which is involved in regulating gene expression,
298 p3 mediated by the histone acetyltransferase Tip60, which targeted Foxp3 for proteasomal degradation.
299 by RNF168 inhibits chromatin acetylation by TIP60, while this residue can be acetylated by TIP60 in