ライフサイエンスコーパス: Tip60

1 ltransferase tat-interactive protein 60 kDa (Tip60).

2 expression of GRIP1 synergizes the action of Tip60.

3 reases the ability of ATXN1 to interact with Tip60.

4 n methylation and acetylation of p53 through Tip60.

5 recruitment of the histone acetyltransferase Tip60.

6 TXN1, RORalpha, and the RORalpha coactivator Tip60.

7 r, and Trrap were also able to interact with Tip60.

8 e activation of ATM and its association with Tip60.

9 the MYST family acetyltransferases hMOF and TIP60.

10 P/Tip60 or after knockdown of endogenous APP/Tip60.

11 iator and a p53 activator, is a regulator of Tip60.

12 methylase LSD1 and histone acetyltransferase Tip60.

13 through the action of the acetyltransferase Tip60.

14 promoting USP7-mediated deubiquitination of Tip60.

15 ir via HRR; effectively phenocopying loss of TIP60.

16 -mediated p53 and lysine acetyl transferase, Tip60.

17 mimic" GK-X-GK motif that is diacetylated by Tip60.

18 es degradation-independent ubiquitination of TIP60.

19 and this is partly due to destabilization of Tip60.

20 dependent apoptotic pathway by destabilizing Tip60.

21 The histone acetyltransferase TIP60, a frequent target of monoallelic loss in human ca

22 ATM mediates the interaction between ATM and Tip60, a histone acetyltransferase that regulates activa

23 Tip60 acetylates the p53 tumor suppressor at lysine 120

24 PARP activities mechanistically by directing Tip60 acetylation of histone H2A lysine 5 at the 5' end

25 The NuA4/TIP60 acetyltransferase complex is a key regulator of ge

26 and that the interaction is dependent on the TIP60 acetyltransferase domain and c-Myb transactivation

27 WI/SNF ATPase and histone acetylation by the Tip60 acetyltransferase.

28 mbers of the MYST (MOZ, Ybf2/Sas3, Sas2, and TIP60) acetyltransferase family, hMOF and TIP60, are SIR

29 Chromatin-monitoring KAT5 (Tip60) acetyltransferase was responsible for acetylation

30 ce the degradation of Tip60, suggesting that Tip60 action may not be required for activation of the A

31 ifferent estrogenic compounds can modify the Tip60 action.

32 ur studies demonstrate that STAT-5 regulates Tip60 activation and this occurs in part by targeting gl

33 UV damage, which is critically important for TIP60 activation.

34 deacetylates TIP60 and negatively regulates TIP60 activity in vivo.

35 The Tip60 activity is modulated by post-translational modifi

36 hin a distinct complex that presumably lacks TIP60 and appears to be involved in the transcriptional

37 he histone acetyltransferase (HAT) domain of TIP60 and blocks both its enzymatic activity and its coa

38 The coincident function of Tip60 and FANCD2 in one pathway is supported by the find

39 A minimum FOXP3 ensemble containing native TIP60 and HDAC7 is necessary for IL-2 production regulat

40 ificantly decreased the association of KLF4, Tip60 and HDAC7 with HDC promoter, suggesting that gastr

41 In addition, Tip60 and HDAC7, previously shown to interact with each

42 as a scaffolding protein for both Dnmt1 and Tip60 and is required for Tip60-mediated acetylation of

43 inal activation domain associates with TRRAP/TIP60 and mixed-lineage-leukemia (MLL1/MLL2) SET1-type c

44 ntified SIRT1 that specifically deacetylates TIP60 and negatively regulates TIP60 activity in vivo.

45 ation, we found that the interaction between TIP60 and p53 is severely inhibited in the presence of U

46 nner that depends on phosphorylation of both Tip60 and PRAK by p38.

47 re critical for the prosenescent function of Tip60 and PRAK, respectively.

48 zymatic activity and biological functions of Tip60 and PRAK.

49 ases HDAC1 and HDAC2, known to interact with TIP60 and repress transcription.

50 GAS41 is a common subunit of the TIP60 and SRCAP complexes and is essential for cell grow

51 nsient transfection assessments showing that Tip60 and SRF cooperatively activate the atrial natriure

52 at UHRF1 is a critical negative regulator of TIP60 and suggest that UHRF1-mediated effects on p53 may

53 ATM blocked the interaction between ATM and Tip60 and suppressed the activation of ATM kinase activi

54 NA-associated AGO2 interacted with MMSET and Tip60 and that the diRNA binding and catalytic activitie

55 d potential regulatory relationships between TIP60 and the c-Myb oncoprotein in hematopoietic cells.

56 exes control access of factors such as E2F1, Tip60, and HDAC1/2/3 to the promoters of various cell-cy

57 sttranslational modifications involving p38, Tip60, and PRAK, three proteins that are essential for r

58 as assessed by crossing ATXN1[82Q] mice with Tip60(+/-)animals.

59 rt here that isoproteins recognized by a pan-Tip60 antibody are strongly and transiently expressed be

60 component of SAGA and the domino subunit of Tip60 are also required for mastermind function during w

61 umor suppressor as mice that are haploid for Tip60 are predisposed to tumors.

62 nd TIP60) acetyltransferase family, hMOF and TIP60, are SIRT1 substrates.

63 Thus, we have identified Tip60 as the first dual-function coregulator of ERbeta1.

64 d Galpha subunits, was sufficient to mediate Tip60 association with RGS6.

65 ATF3 directly binds Tip60 at a region adjacent to the catalytic domain to pr

66 n, we showed the co-occupancy of ERbeta1 and Tip60 at ERE and AP-1 sites of ERbeta1 target genes.

67 The corepressor activity of Tip60 at the ERE site is abolished by diarylpropionitril

68 Taken together, our data reveal TIP60 autoacetylation as a key step in the control of it

69 Mechanistically we demonstrated that TIP60 autoacetylation leads to the dissociation of TIP60

70 A ChIP assay also revealed that TIP60 binds to the c-Myb target gene c-Myc promoter in a

71 TIP60 binds to the HPV major early promoter and acetylat

72 Tip60 binds to the immediate early adenovirus promoter a

73 HD and RING finger domains 1) interacts with TIP60 both in vitro and in vivo and induces degradation-

74 that USP7 interacts with and deubiquitinates Tip60 both in vitro and in vivo.

75 t human papillomavirus (HPV) E6 destabilizes TIP60 both in vivo and in vitro.

76 Overexpression of TIP60 but not its histone acetyltransferase-deficient mu

77 gate the repression of catalytic activity of TIP60 by another protein in TIP60.com, p400.

78 Destabilization of TIP60 by HPV E6 also relieves cellular promoters from TI

79 Thus, degradation of Tip60 by the adenoviral early proteins is important for

80 Thus, degradation of Tip60 by the adenoviral early proteins is important for

81 lt from changes in TIP60 complex assembly or TIP60 coactivator functions for p53, since a TIP60 compl

82 for the lysine acetyltransferase activity of TIP60.com but not for that of the pure recombinant TIP60

83 RVBs are also required for heat stability of TIP60.com by a p400-independent pathway.

84 TIP60 complex (TIP60.com) is a tumor suppressor chromatin-remodeling co

85 ytic activity of TIP60 by another protein in TIP60.com, p400.

86 describe two molecular functions of RVBs in TIP60.com.

87 TIP60 complex (TIP60.com) is a tumor suppressor chromati

88 p53 pathway does not result from changes in TIP60 complex assembly or TIP60 coactivator functions fo

89 g enzyme, exists as an integral subunit of a TIP60 complex but also resides within a distinct complex

90 TIP60 coactivator functions for p53, since a TIP60 complex containing a coiled-coil mutant of GAS41 r

91 The NuA4-Tip60 complex creates these flexible chromatin structure

92 activity of Tip60/NuA4, implicating the Rvb1-Tip60 complex in the chromatin-remodeling response of ce

93 We find that the TIP60 complex regulates association of 53BP1 partly by c

94 ort a model in which NPAT recruits the TRRAP-Tip60 complex to histone gene promoters to coordinate th

95 r an intricate mechanism orchestrated by the TIP60 complex to regulate 53BP1-dependent repair through

96 ns MLL-like complex cooperates with the NuA4/TIP60 complex to regulate the expression of a novel effe

97 ting acetylation of the H4 tail (by the NuA4-Tip60 complex) and shifting the chromatin to a more open

98 tone acetyltransferase (HAT) activity of the Tip60 complex, and histone H4 acetylation is required pr

99 ein (TRRAP) and Tip60, two components of the Tip60 complex, associate with histone gene promoters at

100 d with mutations in the Trrap subunit of the TIP60 complex, both in the cell line panel and in a huma

101 orrelation with the association of the TRRAP-Tip60 complex, histone H4 acetylation at histone gene pr

102 ility to methylate RUVBL1, a cofactor of the TIP60 complex.

103 omplex, cohesion, DNA-PKcs and components of TIP60 complex.

104 ssembly, heat stability, and function of the TIP60 complex.

105 hromatin remodeling SRCAP, hINO80, and TRRAP/TIP60 complexes, and the nutrient sensing complex Uri/Pr

106 Nipped-A, through the action of the SAGA and Tip60 complexes, facilitates assembly of the Notch activ

107 Here, we describe a TIP60-containing p400 complex population in which the ac

108 the histone acetyltransferase complex, NuA4/TIP60, cooperates with the C. elegans MLL-like complex i

109 We then found that coexpressing TIP60 decreases the transcriptional activation ability o

110 It was previously suggested that TIP60-dependent acetylation of H4 regulates binding of t

111 Thus, our study demonstrates that Tip60-dependent acetylation of p53 at K120 modulates the

112 DMAP1 associated with TIP60-dependent HAT activity, and depletion of DMAP1 red

113 thway, which is preliminarily activated by a Tip60-dependent mechanism in response to chromatin relax

114 hylation at position R205, which facilitates TIP60-dependent mobilization of 53BP1 from DNA breaks, p

115 Notably, p90 is crucial for Tip60-dependent p53 acetylation at Lys120, therefore fac

116 protein that binds H4K12ac, phenocopies the Tip60 depletion with respect to heterochromatin decompac

117 Tip60 depletion, but not Ino80 or SRCAP depletion, mimic

118 However, depletion of Tip60 did not reduce monoubiquitination of FANCD2 or its

119 Tip60 differentially regulates the endogenous expression

120 ults suggested a specific, temporal role for Tip60 during disease progression.

121 In this study, we found that Tip60 enhances transactivation of ERbeta1 at the AP-1 si

122 anisms that include the direct inhibition of TIP60 enzymatic activity described here and the previous

123 The histone acetyltransferase (HAT) Tip60 epigenetically regulates genes enriched for neuron

124 mediated by APP and that, remarkably, excess Tip60 exerts a neuroprotective role in APP-induced axona

125 ckdown of ATF3 expression leads to decreased Tip60 expression and suppression of ATM signalling as ev

126 Suppression of TRRAP or Tip60 expression by RNA interference inhibits histone ge

127 Consistently, knockdown of Tip60 expression by siRNA increased endogenous c-Myc exp

128 Finally, we compared Tip60 expression in six primary AML samples with three n

129 no significant difference in SRC-1, p300, or TIP60 expression was found.

130 Tip60 expression was significantly ( approximately 60%)

131 When Tip60 expression was suppressed by small interfering RNA

132 ome recognition by the MOZ, Ybf2/Sas3, Sas2, Tip60 family HAT complex, Piccolo NuA4 (picNuA4).

133 1), a member of the MYST (Moz-Ybf2/Sas3-Sas2-Tip60) family of histone acetyltransferases (HATs), is t

134 d methylation at p53 K372 directly activates Tip60 for its catalyzed acetylation at p53 K120.

135 erminal 106-190 aa of FOXP3 are required for TIP60-FOXP3, HDAC7-FOXP3 association, as well as for the

136 oth endogenous and epitope-tagged FANCD2 and Tip60 from human cells.

137 Finally, we demonstrate that Tip60 function in axonal transport is mediated by APP an

138 on of a common stress mediator in regulating Tip60 function.

139 Tip60beta (which lacks exon V encoded by the Tip60 gene), and Tip55 (which encodes a novel 103-amino-

140 Although Tip60 has been shown to interact with both receptors, it

141 a novel functional interactive role between Tip60 HAT activity and APP in axonal transport and provi

142 Here, we examine whether Tip60 HAT activity functions in axonal transport using D

143 We show that reduction of Tip60 HAT activity in the nervous system causes axonopat

144 ing genetic approaches, we show that loss of Tip60 HAT activity in the presence of the Alzheimer's di

145 Here, we show that Tip60 HAT activity mediates axonal growth of the Drosoph

146 onents of the SRCAP chromatin remodeling and TIP60 HAT complexes, whereas the small complex possesses

147 Moreover, the Tip60/HAT inhibitor, NU9056, was able to block EtOH-indu

148 These studies indicate RORalpha and Tip60 have a role in SCA1 and suggest a mechanism by whi

149 Several alternative splice variants of Tip60 have been characterized, including full-length Tip

150 t partly by decreasing the formation of KLF4/Tip60/HDAC7 repressive complexes at the HDC promoter.

151 In embryonic stem cells (ESCs), the Tip60 histone acetyltransferase activates genes required

152 w that NPAT interacts with components of the Tip60 histone acetyltransferase complex through a novel

153 ibed OFD1 interactors were components of the TIP60 histone acetyltransferase complex.

154 CX as well as EP400, a component of the NuA4/TIP60 histone acetyltransferase complex.

155 The TIP60 histone acetyltransferase plays diverse roles in D

156 3016 of ATM is a substrate in vitro for the Tip60 histone acetyltransferase.

157 activity involves acetylation of ATM by the Tip60 histone acetyltransferase.

158 erefore function as a binding domain for the Tip60 histone acetyltransferase.

159 a reader protein of H3K36me3, and the KAT5 (TIP60) histone acetyltransferase.

160 TIP60 (HTATIP) is a histone acetyltransferase (HAT) whos

161 siently interrupted, with corresponding hMOF/TIP60 hyperacetylation.

162 Notably, overexpression of Tip60 in conjunction with APP rescues these sleep-wake d

163 s supported by the finding that depletion of Tip60 in Fanconi anemia cells does not increase sensitiv

164 he kinase GSK3beta mediate the activation of Tip60 in HPV-positive cells.

165 ctivity is required for the stabilization of Tip60 in order to operate an effective p53-dependent apo

166 ssion is associated with mis-localization of TIP60 in patient-derived cell lines.

167 was inhibited, demonstrating a key role for Tip60 in the activation of DNA-PKcs by DNA damage.

168 fication, demonstrating the critical role of Tip60 in the viral life cycle.

169 through phosphorylation of Thr158; activated Tip60 in turn directly interacts with and induces the pr

170 Moreover, Ran was acetylated by CBP/p300 and Tip60 in vitro and on transferase overexpression in vivo

171 P60, while this residue can be acetylated by TIP60 in vivo, blocking its ubiquitylation.

172 Tip60, in turn, acetylates p53, thereby restoring p53-me

173 rotein acetyltransferase KAT5 (also known as TIP60) increases after DNA damage in a manner that promo

174 or pathway during the normal cell cycle by a TIP60-independent mechanism.

175 tomycin C in normal fibroblasts depleted for Tip60 indicates a direct function in interstrand cross-l

176 nsistent with this, depletion of hMOF and/or TIP60 inhibits the ability of p53 to activate BAX and PU

177 ylation of the enzymatic domains of hMOF and TIP60 inhibits their acetyltransferase activity and prom

178 HPV E6 also relieves cellular promoters from TIP60-initiated repression and abrogates p53-dependent a

179 ATXN1 and Tip60 interact directly via the ATXN1 and HMG-box protei

180 Moreover, the ATF3-Tip60 interaction increases the Tip60 stability by promo

181 roach, the biological relevance of the ATXN1/Tip60 interaction was assessed by crossing ATXN1[82Q] mi

182 find that the chromatin remodeling protein, Tip60, interacts directly with the FANCD2 protein in a y

183 rther show that AICD, together with Fe65 and Tip60, interacts with the LRP1 promoter and suppresses i

184 Tip60 is a bona fide tumor suppressor as mice that are h

185 We first showed that TIP60 is a c-Myb interacting protein and that the intera

186 The histone acetyltransferase TIP60 is a coregulator of transcription factors and is i

187 Tip60 is a histone acetyltransferase (HAT) enzyme that e

188 in response to DNA damage demonstrates that Tip60 is a key component of the DNA damage-signaling net

189 Although Tip60 is a known acetyltransferase, it is unable to acet

190 Tip60 is a lysine acetyltransferase that acetylates hist

191 oietic cells, leading us to hypothesize that TIP60 is a normal regulator of c-Myb function and that d

192 Tip60 is an essential acetyltransferase required for ace

193 Here we showed that TIP60 is autoacetylated in response to UV damage, which

194 oprecipitation experiments demonstrated that Tip60 is constitutively associated with DNA-PKcs and tha

195 We have discovered that Tip60 is degraded by adenovirus oncoproteins EIB55K and

196 is defective, the histone acetyltransferase Tip60 is recruited to pericentric heterochromatin, where

197 n in which the acetyltransferase activity of TIP60 is repressed by interactions with p400.

198 Here, we show that Tip60 is required for both cell growth arrest and apopto

199 The acetylation of ATM on lysine 3016 by Tip60 is therefore a key step linking the detection of D

200 DNA damage, the binding of SIRT1 to hMOF and TIP60 is transiently interrupted, with corresponding hMO

201 It is known that Tip60 is turned over in cells by the ubiquitin-proteasom

202 the deubiquitinase activity for stabilizing Tip60 is unknown.

203 Tat-interactive protein 60 (Tip60) is a member of the MYST family of histone acetylt

204 Tat-interactive protein 60 (Tip60) is a MYST histone acetyltransferase that catalyse

205 A functional role for Tip60 isoproteins in cardiac myocyte differentiation is

206 rase MMSET (WHSC1) and the acetyltransferase Tip60 (KAT5) to the DSB, where local levels of histone H

207 g of Saccharomyces cerevisiae Esa1 and human Tip60 (KAT5).

208 s to H4Ac, which is generated at DSBs by the Tip60/KAT5 acetyltransferase.

209 HP10 colocalize to nuclear foci positive for TIP60, known to activate ATM at sites of DNA damage.

210 by reduced locomotion activity of the mutant Tip60 larvae, and these phenotypes can be partially resc

211 Furthermore, in such a context, depletion of Tip60 leads to derepression of satellite transcription,

212 Our study indicates that Tip60 levels and activity are increased in cells that st

213 ATF2 expression is inversely correlated with TIP60 levels and ATM activation after IR.

214 Partial Tip60 loss increased Rora and Rora-mediated gene express

215 yb function and that dysregulated or mutated TIP60 may contribute to c-Myb-driven leukemogenesis.

216 Our findings reveal a novel mechanism for Tip60 mediated sleep-wake regulation via control of axon

217 for both Dnmt1 and Tip60 and is required for Tip60-mediated acetylation of Dnmt1 and subsequent Dnmt1

218 In addition, TIP60-mediated acetylation of nucleosomal H2A specifical

219 uced cellular transformation by facilitating Tip60-mediated degradation of Dmnt1 and promoting apopto

220 Nevertheless, it remains unclear how TIP60-mediated effects on p53 are dynamically regulated

221 However, whether Tip60-mediated epigenetic dysregulation affects specific

222 ce of UHRF1, suggesting that UHRF1 modulates TIP60-mediated functions in both K120 acetylation-depend

223 for p53-mediated apoptosis through promoting Tip60-mediated p53 acetylation.

224 the possibility that an epigenetic role for Tip60 might also be involved.

225 These findings suggest that Tip60 modulates expression of SRF-dependent cardiac gene

226 , following DNA damage the acetyltransferase Tip60 must acetylate ATM proteins prior to their full ac

227 inger (MOZ)/KAT6A is a MOZ, Ybf2/Sas3, Sas2, Tip60 (MYST)-type histone acetyltransferase that functio

228 In summary, these studies demonstrate that TIP60 negatively modulates c-Myb transcriptional activit

229 and is a key component of both the SAGA and Tip60 (NuA4) chromatin-modifying complexes.

230 2-related CBP activator protein (SRCAP), and Tip60/NuA4 complexes, but their molecular function is un

231 r to members of the Myb-MuvB/dREAM, NuRD and Tip60/NuA4 complexes.

232 e of Rvb1 in maintaining the HAT activity of Tip60/NuA4, implicating the Rvb1-Tip60 complex in the ch

233 omplexes similar to Myb-MuvB/dREAM, NuRD and Tip60/NuA4.

234 We propose that the underexpression of Tip60 observed in many human tumors can promote genetic

235 autoacetylation leads to the dissociation of TIP60 oligomer and enhances its interaction with substra

236 ATF2 association with TIP60 on chromatin is decreased following exposure to io

237 in the presence or absence of exogenous APP/Tip60 or after knockdown of endogenous APP/Tip60.

238 Consistently, knock down of Tip60 or HDAC7 gene expression by specific shRNA increas

239 Inhibition of either STAT-5, Tip60, or GSK3beta blocked differentiation-dependent gen

240 etylate histones, but rather is required for Tip60-p400 binding to many of its target genes.

241 I histone deacetylase Hdac6 co-purifies with Tip60-p400 complex from ESCs.

242 MT1-associated protein 1) is a member of the TIP60-p400 complex that maintains embryonic stem (ES) ce

243 e phenotypes of loss of other members of the TIP60-p400 complex, Dmap1(-/-) mice died during preimpla

244 ckdown (KD), including seven subunits of the Tip60-p400 complex.

245 dac6 plays a major role in the modulation of Tip60-p400 function in stem cells.

246 ociated protein 1 (DMAP1) is a member of the TIP60-p400 histone acetyl transferase (HAT) complex, whi

247 d some cancer cell lines, and interacts with Tip60-p400 in each.

248 Hdac6 localizes to promoters bound by Tip60-p400 in ESCs, binding downstream of transcription

249 Together, these data indicate that Tip60-p400 integrates signals from Nanog and H3K4me3 to

250 Phenotypic analyses revealed that Tip60-p400 is necessary to maintain characteristic featu

251 Furthermore, the Tip60-p400 KD gene expression profile is enriched for de

252 antation epigenetic reprogramming processes: TIP60-p400 nucleosome remodeling and DNMT1 maintenance m

253 Hdac6 is necessary for regulation of most Tip60-p400 target genes, particularly those repressed by

254 ly, we find that, like canonical subunits of Tip60-p400, Hdac6 is necessary for robust ESC differenti

255 Fe65, Tip60, p53, and caspases play a role in tau-independent

256 TIP60 plays important roles in controlling DNA repair.

257 We investigated what role, if any, Tip60 plays in regulating the differentiation-dependent

258 te that a multifunctional acetyltransferase, Tip60, plays an essential role in oncogenic ras-induced

259 ly displace the SNF2 domain of p400 from the TIP60 polypeptide.

260 com but not for that of the pure recombinant TIP60 polypeptide.

261 ted in primary human regulatory T cells, and TIP60 promotes FOXP3 acetylation in vivo.

262 quired for the acetyltransferase activity of TIP60, promoting histone H4K16 acetylation, which facili

263 n of ATF2 expression in these lines restored TIP60 protein levels and both basal and IR-induced level

264 sion by small interfering RNA stabilizes the TIP60 protein.

265 nt promotes, whereas knockdown of endogenous TIP60 relieved, FOXP3-mediated transcriptional repressio

266 (PP2A)B subunit, Tat-interactive protein 60 (TIP60), replication protein A1 (RPA1), and RPA2 proteins

267 ations in SIRT1-targeted lysines on hMOF and TIP60 repress DNA double-strand break repair and inhibit

268 TIP60 resides within a multisubunit complex that has bee

269 LANA-associated TIP60 retained acetyltransferase activity and, unlike hu

270 nizing radiation (IR), resulting in enhanced TIP60 stability and activity.

271 ATM activation by ATF2-dependent control of TIP60 stability and activity.

272 er, the ATF3-Tip60 interaction increases the Tip60 stability by promoting USP7-mediated deubiquitinat

273 and HIV-1 TAT proteins, LANA did not reduce TIP60 stability.

274 complex possesses only a subset of SRCAP and TIP60 subunits.

275 howed that HDAC7 was pulled down by KLF4 and Tip60, suggesting that these three proteins form a repre

276 have been shown to induce the degradation of Tip60, suggesting that Tip60 action may not be required

277 egulation of certain axonal transport-linked Tip60 target genes.

278 We and others previously showed that TIP60 (Tat-interacting protein of 60 kDa)-mediated acety

279 plex that includes histone acetyltransferase TIP60 (Tat-interactive protein, 60 kDa) and class II his

280 alian pericentric heterochromatin relying on Tip60 that might be dependent on BRD2 recruitment by H4K

281 interact with the histone acetyltransferase Tip60, the histone deacetylase HDAC7, and the Ikaros fam

282 ion and glucose production were dependent on TIP60, the human homolog of ESA1.

283 ul3 ubiquitin ligase promotes degradation of TIP60, thereby attenuating its HAT activity.

284 Both low- and high-risk HPV E6 destabilize TIP60, thereby derepressing their own promoter.

285 Degradation of TIP60, therefore, allows low- and high-risk HPV to promo

286 ically interacts with and regulates hMOF and TIP60 through deacetylation and provide additional mecha

287 38 induces the acetyltransferase activity of Tip60 through phosphorylation of Thr158; activated Tip60

288 xpression markedly suppresses the ability of TIP60 to acetylate p53.

289 e reader domain for H4K20me1/2, MBTD1 allows TIP60 to associate with specific gene promoters and to p

290 Taken together, our findings identify Tip60 to be an important regulator of HPV genome amplifi

291 ut required for the recruitment of MMSET and Tip60 to DSBs.

292 L1 methylation did not affect the ability of TIP60 to facilitate ATM activation.

293 break repair and inhibit the ability of hMOF/TIP60 to induce apoptosis in response to DNA double-stra

294 red for the binding of the acetyltransferase Tip60 to p53 and for the subsequent acetylation of p53.

295 Further, the ability of Tip60 to regulate the activation of both ATM and DNA-PKc

296 The TIP60 tumor suppressor is a histone acetyltransferase in

297 vation domain-associated protein (TRRAP) and Tip60, two components of the Tip60 complex, associate wi

298 study, by using yeast two-hybrid screening, Tip60 was identified as a KLF4 interacting protein.

299 p3 mediated by the histone acetyltransferase Tip60, which targeted Foxp3 for proteasomal degradation.

300 by RNF168 inhibits chromatin acetylation by TIP60, while this residue can be acetylated by TIP60 in

301 Knockdown of Tip60 with short hairpin RNAs in cells that maintain HPV