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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.
15                The histone acetyltransferase TIP60, a frequent target of monoallelic loss in human ca
16    We show that the lysine acetyltransferase Tip60 acetylates eEF1A1, whereas the histone deacetylase
17                                              Tip60 acetylates the p53 tumor suppressor at lysine 120
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
21                                     The NuA4/TIP60 acetyltransferase complex is a key regulator of ge
22 and that the interaction is dependent on the TIP60 acetyltransferase domain and c-Myb transactivation
23 WI/SNF ATPase and histone acetylation by the Tip60 acetyltransferase.
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
26                   Chromatin-monitoring KAT5 (Tip60) acetyltransferase was responsible for acetylation
27 ce the degradation of Tip60, suggesting that Tip60 action may not be required for activation of the A
28 ifferent estrogenic compounds can modify the Tip60 action.
29 ur studies demonstrate that STAT-5 regulates Tip60 activation and this occurs in part by targeting gl
30 UV damage, which is critically important for TIP60 activation.
31  deacetylates TIP60 and negatively regulates TIP60 activity in vivo.
32                                          The Tip60 activity is modulated by post-translational modifi
33 hin a distinct complex that presumably lacks TIP60 and appears to be involved in the transcriptional
34                 Consequently, recruitment of TIP60 and ATM, two key proximal HDR factors, is substant
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
37                   The coincident function of Tip60 and FANCD2 in one pathway is supported by the find
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
40                                 In addition, Tip60 and HDAC7, previously shown to interact with each
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
45 nner that depends on phosphorylation of both Tip60 and PRAK by p38.
46 re critical for the prosenescent function of Tip60 and PRAK, respectively.
47 zymatic activity and biological functions of Tip60 and PRAK.
48 ases HDAC1 and HDAC2, known to interact with TIP60 and repress transcription.
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
54 as assessed by crossing ATXN1[82Q] mice with Tip60(+/-)animals.
55 umor suppressor as mice that are haploid for Tip60 are predisposed to tumors.
56 nd TIP60) acetyltransferase family, hMOF and TIP60, are SIRT1 substrates.
57                   In this study, we identify TIP60 as a novel upstream regulator of DeltaNp63alpha.
58                     Thus, we have identified Tip60 as the first dual-function coregulator of ERbeta1.
59 d Galpha subunits, was sufficient to mediate Tip60 association with RGS6.
60                          ATF3 directly binds Tip60 at a region adjacent to the catalytic domain to pr
61 n, we showed the co-occupancy of ERbeta1 and Tip60 at ERE and AP-1 sites of ERbeta1 target genes.
62                  The corepressor activity of Tip60 at the ERE site is abolished by diarylpropionitril
63              Taken together, our data reveal TIP60 autoacetylation as a key step in the control of it
64         Mechanistically we demonstrated that TIP60 autoacetylation leads to the dissociation of TIP60
65              A ChIP assay also revealed that TIP60 binds to the c-Myb target gene c-Myc promoter in a
66                                              TIP60 binds to the HPV major early promoter and acetylat
67                                              Tip60 binds to the immediate early adenovirus promoter a
68 HD and RING finger domains 1) interacts with TIP60 both in vitro and in vivo and induces degradation-
69 that USP7 interacts with and deubiquitinates Tip60 both in vitro and in vivo.
70 t human papillomavirus (HPV) E6 destabilizes TIP60 both in vivo and in vitro.
71 ing activities and repair factors, including Tip60, BRG1 and NBS1, and renders mice hypersensitive to
72                            Overexpression of TIP60 but not its histone acetyltransferase-deficient mu
73 gate the repression of catalytic activity of TIP60 by another protein in TIP60.com, p400.
74                           Destabilization of TIP60 by HPV E6 also relieves cellular promoters from TI
75                         Thus, degradation of Tip60 by the adenoviral early proteins is important for
76                         Thus, degradation of Tip60 by the adenoviral early proteins is important for
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
79                       We further showed that TIP60 coexpression inhibits DeltaNp63alpha ubiquitinatio
80 for the lysine acetyltransferase activity of TIP60.com but not for that of the pure recombinant TIP60
81 RVBs are also required for heat stability of TIP60.com by a p400-independent pathway.
82                               TIP60 complex (TIP60.com) is a tumor suppressor chromatin-remodeling co
83 ytic activity of TIP60 by another protein in TIP60.com, p400.
84  describe two molecular functions of RVBs in TIP60.com.
85                                              TIP60 complex (TIP60.com) is a tumor suppressor chromati
86 g enzyme, exists as an integral subunit of a TIP60 complex but also resides within a distinct complex
87                                     The NuA4-Tip60 complex creates these flexible chromatin structure
88 activity of Tip60/NuA4, implicating the Rvb1-Tip60 complex in the chromatin-remodeling response of ce
89                             We find that the TIP60 complex regulates association of 53BP1 partly by c
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
98 ssembly, heat stability, and function of the TIP60 complex.
99 ility to methylate RUVBL1, a cofactor of the TIP60 complex.
100 omplex, cohesion, DNA-PKcs and components of TIP60 complex.
101 hromatin remodeling SRCAP, hINO80, and TRRAP/TIP60 complexes, and the nutrient sensing complex Uri/Pr
102                          Here, we describe a TIP60-containing p400 complex population in which the ac
103  the histone acetyltransferase complex, NuA4/TIP60, cooperates with the C. elegans MLL-like complex i
104              We then found that coexpressing TIP60 decreases the transcriptional activation ability o
105             It was previously suggested that TIP60-dependent acetylation of H4 regulates binding of t
106 findings reveal that phosphorylation directs TIP60-dependent acetylation to promote homologous recomb
107                        DMAP1 associated with TIP60-dependent HAT activity, and depletion of DMAP1 red
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
110                  Notably, p90 is crucial for Tip60-dependent p53 acetylation at Lys120, therefore fac
111  protein that binds H4K12ac, phenocopies the Tip60 depletion with respect to heterochromatin decompac
112                                              Tip60 depletion, but not Ino80 or SRCAP depletion, mimic
113                        However, depletion of Tip60 did not reduce monoubiquitination of FANCD2 or its
114                                              Tip60 differentially regulates the endogenous expression
115 ults suggested a specific, temporal role for Tip60 during disease progression.
116                 In this study, we found that Tip60 enhances transactivation of ERbeta1 at the AP-1 si
117 anisms that include the direct inhibition of TIP60 enzymatic activity described here and the previous
118 y deleting Ep400, the central subunit of the Tip60/Ep400 complex.
119          The histone acetyltransferase (HAT) Tip60 epigenetically regulates genes enriched for neuron
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
122                      Suppression of TRRAP or Tip60 expression by RNA interference inhibits histone ge
123                   Consistently, knockdown of Tip60 expression by siRNA increased endogenous c-Myc exp
124                         Finally, we compared Tip60 expression in six primary AML samples with three n
125 no significant difference in SRC-1, p300, or TIP60 expression was found.
126                                              Tip60 expression was significantly ( approximately 60%)
127 ome recognition by the MOZ, Ybf2/Sas3, Sas2, Tip60 family HAT complex, Piccolo NuA4 (picNuA4).
128 1), a member of the MYST (Moz-Ybf2/Sas3-Sas2-Tip60) family of histone acetyltransferases (HATs), is t
129 d methylation at p53 K372 directly activates Tip60 for its catalyzed acetylation at p53 K120.
130 erminal 106-190 aa of FOXP3 are required for TIP60-FOXP3, HDAC7-FOXP3 association, as well as for the
131 oth endogenous and epitope-tagged FANCD2 and Tip60 from human cells.
132                 Finally, we demonstrate that Tip60 function in axonal transport is mediated by APP an
133 on of a common stress mediator in regulating Tip60 function.
134                                     Although Tip60 has been shown to interact with both receptors, it
135  a novel functional interactive role between Tip60 HAT activity and APP in axonal transport and provi
136                     Here, we examine whether Tip60 HAT activity functions in axonal transport using D
137                    We show that reduction of Tip60 HAT activity in the nervous system causes axonopat
138 ing genetic approaches, we show that loss of Tip60 HAT activity in the presence of the Alzheimer's di
139                           Here, we show that Tip60 HAT activity mediates axonal growth of the Drosoph
140 o promote transcription through SAGA DUB and Tip60 HAT activity.
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.
143                                   Increasing Tip60 HAT levels specifically in the mushroom body learn
144          We show that like AD, disruption of Tip60 HAT/HDAC2 balance with concomitant epigenetic repr
145                                Moreover, the Tip60/HAT inhibitor, NU9056, was able to block EtOH-indu
146 t partly by decreasing the formation of KLF4/Tip60/HDAC7 repressive complexes at the HDC promoter.
147          In embryonic stem cells (ESCs), the Tip60 histone acetyltransferase activates genes required
148 w that NPAT interacts with components of the Tip60 histone acetyltransferase complex through a novel
149 CX as well as EP400, a component of the NuA4/TIP60 histone acetyltransferase complex.
150 ibed OFD1 interactors were components of the TIP60 histone acetyltransferase complex.
151                                          The TIP60 histone acetyltransferase plays diverse roles in D
152 ontin functions as a platform for recruiting Tip60 histone acetyltransferase with increased H4 acetyl
153  3016 of ATM is a substrate in vitro for the Tip60 histone acetyltransferase.
154  activity involves acetylation of ATM by the Tip60 histone acetyltransferase.
155 IPPED-A protein, a scaffold for the SAGA and Tip60 histone modifying complexes, interacts with GFP-CL
156  a reader protein of H3K36me3, and the KAT5 (TIP60) histone acetyltransferase.
157                                              TIP60 (HTATIP) is a histone acetyltransferase (HAT) whos
158 siently interrupted, with corresponding hMOF/TIP60 hyperacetylation.
159                   Notably, overexpression of Tip60 in conjunction with APP rescues these sleep-wake d
160 s supported by the finding that depletion of Tip60 in Fanconi anemia cells does not increase sensitiv
161 he kinase GSK3beta mediate the activation of Tip60 in HPV-positive cells.
162 ctivity is required for the stabilization of Tip60 in order to operate an effective p53-dependent apo
163 ssion is associated with mis-localization of TIP60 in patient-derived cell lines.
164 fication, demonstrating the critical role of Tip60 in the viral life cycle.
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
168 P60, while this residue can be acetylated by TIP60 in vivo, blocking its ubiquitylation.
169                                              Tip60, in turn, acetylates p53, thereby restoring p53-me
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
174                                    ATXN1 and Tip60 interact directly via the ATXN1 and HMG-box protei
175                           Moreover, the ATF3-Tip60 interaction increases the Tip60 stability by promo
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
179                                              Tip60 is a bona fide tumor suppressor as mice that are h
180                         We first showed that TIP60 is a c-Myb interacting protein and that the intera
181                The histone acetyltransferase TIP60 is a coregulator of transcription factors and is i
182                                              Tip60 is a histone acetyltransferase (HAT) enzyme that e
183                                     Although Tip60 is a known acetyltransferase, it is unable to acet
184                                              Tip60 is a lysine acetyltransferase that acetylates hist
185 oietic cells, leading us to hypothesize that TIP60 is a normal regulator of c-Myb function and that d
186                                              Tip60 is an essential acetyltransferase required for ace
187                          Here we showed that TIP60 is autoacetylated in response to UV damage, which
188                      We have discovered that Tip60 is degraded by adenovirus oncoproteins EIB55K and
189  is defective, the histone acetyltransferase Tip60 is recruited to pericentric heterochromatin, where
190 n in which the acetyltransferase activity of TIP60 is repressed by interactions with p400.
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
193                             It is known that Tip60 is turned over in cells by the ubiquitin-proteasom
194  the deubiquitinase activity for stabilizing Tip60 is unknown.
195                  Tat-interactive protein 60 (Tip60) is a MYST histone acetyltransferase that catalyse
196 rase MMSET (WHSC1) and the acetyltransferase Tip60 (KAT5) to the DSB, where local levels of histone H
197 g of Saccharomyces cerevisiae Esa1 and human Tip60 (KAT5).
198 s to H4Ac, which is generated at DSBs by the Tip60/KAT5 acetyltransferase.
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,
202                     Our study indicates that Tip60 levels and activity are increased in cells that st
203 ATF2 expression is inversely correlated with TIP60 levels and ATM activation after IR.
204                                      Partial Tip60 loss increased Rora and Rora-mediated gene express
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
209                                 In addition, TIP60-mediated acetylation of nucleosomal H2A specifical
210 p63alpha protein was further associated with TIP60-mediated acetylation.
211 uced cellular transformation by facilitating Tip60-mediated degradation of Dmnt1 and promoting apopto
212         Nevertheless, it remains unclear how TIP60-mediated effects on p53 are dynamically regulated
213                             However, whether Tip60-mediated epigenetic dysregulation affects specific
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
216 for p53-mediated apoptosis through promoting Tip60-mediated p53 acetylation.
217                Finally, we demonstrated that TIP60-mediated regulation of DeltaNp63alpha increases ce
218  the possibility that an epigenetic role for Tip60 might also be involved.
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
226       We propose that the underexpression of Tip60 observed in many human tumors can promote genetic
227 autoacetylation leads to the dissociation of TIP60 oligomer and enhances its interaction with substra
228                        ATF2 association with TIP60 on chromatin is decreased following exposure to io
229 his study, we report that phosphorylation of TIP60 on serines 90 and 86 is important for limiting the
230                  Consistently, knock down of Tip60 or HDAC7 gene expression by specific shRNA increas
231                 Inhibition of either STAT-5, Tip60, or GSK3beta blocked differentiation-dependent gen
232 etylate histones, but rather is required for Tip60-p400 binding to many of its target genes.
233 I histone deacetylase Hdac6 co-purifies with Tip60-p400 complex from ESCs.
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
236 ckdown (KD), including seven subunits of the Tip60-p400 complex.
237 dac6 plays a major role in the modulation of Tip60-p400 function in stem cells.
238 ociated protein 1 (DMAP1) is a member of the TIP60-p400 histone acetyl transferase (HAT) complex, whi
239 d some cancer cell lines, and interacts with Tip60-p400 in each.
240        Hdac6 localizes to promoters bound by Tip60-p400 in ESCs, binding downstream of transcription
241           Together, these data indicate that Tip60-p400 integrates signals from Nanog and H3K4me3 to
242            Phenotypic analyses revealed that Tip60-p400 is necessary to maintain characteristic featu
243                             Furthermore, the Tip60-p400 KD gene expression profile is enriched for de
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
247                                        Fe65, Tip60, p53, and caspases play a role in tau-independent
248                                              TIP60 plays important roles in controlling DNA repair.
249           We investigated what role, if any, Tip60 plays in regulating the differentiation-dependent
250 te that a multifunctional acetyltransferase, Tip60, plays an essential role in oncogenic ras-induced
251 ly displace the SNF2 domain of p400 from the TIP60 polypeptide.
252 com but not for that of the pure recombinant TIP60 polypeptide.
253 ted in primary human regulatory T cells, and TIP60 promotes FOXP3 acetylation in vivo.
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
257 sion by small interfering RNA stabilizes the TIP60 protein.
258 t with these observations, Nrf1, RUVBL1, and TIP60 proteins were co-recruited to the promoter regions
259 ated histone H4 is important for Suv39h1 and Tip60 recruitment.
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
263                                              TIP60 resides within a multisubunit complex that has bee
264                              LANA-associated TIP60 retained acetyltransferase activity and, unlike hu
265 nizing radiation (IR), resulting in enhanced TIP60 stability and activity.
266  ATM activation by ATF2-dependent control of TIP60 stability and activity.
267 er, the ATF3-Tip60 interaction increases the Tip60 stability by promoting USP7-mediated deubiquitinat
268  and HIV-1 TAT proteins, LANA did not reduce TIP60 stability.
269 complex possesses only a subset of SRCAP and TIP60 subunits.
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
272 egulation of certain axonal transport-linked Tip60 target genes.
273  concomitant epigenetic repression of common Tip60 target neuroplasticity genes occurs early in multi
274         We and others previously showed that TIP60 (Tat-interacting protein of 60 kDa)-mediated acety
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
278 ion and glucose production were dependent on TIP60, the human homolog of ESA1.
279 ul3 ubiquitin ligase promotes degradation of TIP60, thereby attenuating its HAT activity.
280   Both low- and high-risk HPV E6 destabilize TIP60, thereby derepressing their own promoter.
281                               Degradation of TIP60, therefore, allows low- and high-risk HPV to promo
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
284 xpression markedly suppresses the ability of TIP60 to acetylate p53.
285 e reader domain for H4K20me1/2, MBTD1 allows TIP60 to associate with specific gene promoters and to p
286        Taken together, our findings identify Tip60 to be an important regulator of HPV genome amplifi
287 ut required for the recruitment of MMSET and Tip60 to DSBs.
288 L1 methylation did not affect the ability of TIP60 to facilitate ATM activation.
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.
291                                          The TIP60 tumor suppressor is a histone acetyltransferase in
292 vation domain-associated protein (TRRAP) and Tip60, two components of the Tip60 complex, associate wi
293 aches in multiple cell lines, we showed that TIP60 up-regulates DeltaNp63alpha expression.
294  study, by using yeast two-hybrid screening, Tip60 was identified as a KLF4 interacting protein.
295                The histone acetyltransferase TIP60 was previously shown to suppress pathological end
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
300                                 Knockdown of Tip60 with short hairpin RNAs in cells that maintain HPV

 
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