ライフサイエンスコーパス: p73

1 optosis by upregulating the tumor suppressor p73.

2 xhibiting much faster exchange kinetics than p73.

3 y p53 and the related family members p63 and p73.

4 their gain-of-function through NF-Y and p63/p73.

5 an target of rapamycin (mTOR) and inducer of p73.

6 to microRNA-mediated feedback inhibition of p73.

7 ates, expression of endogenous and exogenous p73.

8 s ability to form a complex with NF-Y or p63/p73.

9 ion of the transcriptional activities of p63/p73.

10 tified multiple DNA repair genes affected by p73.

11 otes the proteasome-dependent degradation of p73.

12 d with decreased expression of DeltaNp63 and p73.

13 transactivation was also found with p63 and p73.

14 apoptosis through binding and inhibition of p73.

15 ns, including the p53 family members p63 and p73.

16 lead to apoptosis via activation of p63 and p73.

17 3 mRNA stability via the CU-rich elements in p73 3'-UTR.

18 p73, a member of the p53 family, plays a critical role i

19 aim of this study was to investigate whether p73, a member of the p53 gene family, has a role in the

20 Mdm2 deletion also increased levels of p73, a p53 family member.

21 p73, a p53 family tumor suppressor, is expressed as TA a

22 hlight the previously uncharacterized use of p73-activating therapeutics to target CRCSCs.

23 3 is rarely mutated in colorectal cancer and p73 activation elicits p53-like tumor suppression.

24 porter activation, DeltaNp73 downregulation, p73 activation, and cell death.

25 restores the p53 pathway in tumor cells via p73 activation, on CRCSCs in vitro and in vivo Prodigios

26 SC59984 restores wild-type p53 signaling via p73 activation, specifically in mutant p53-expressing co

27 The p53 isoforms inhibit p53 and p73 activities, induce NF-kappaB, and increase survival

28 3 by p53R175H, but enhance the inhibition of p73 activity by p53R175H and R273H.

29 However, how p73 activity is controlled at the posttranscriptional le

30 Mdm2(Tg);p73(+/-) mice retain the remaining p73 allele, exhibit elevated levels of the antiapoptotic

31 c fibroblasts leads to reduced expression of p73, along with decreased expression of p21, p130, and g

32 Aurora-A phosphorylated p73 also facilitates inactivation of SAC through dissoci

33 Whether the p53 homolog p73 also functions as a tumor suppressor in vivo remains

34 ent, Wilhelm and colleagues demonstrate that p73-an older sibling of p53-inhibits pathways that resol

35 ranscriptional regulator YAP, which binds to p73 and activates its proapoptotic effects.

36 lls of wild-type ventricles strongly express p73 and are particularly vulnerable to p73 deficiency.

37 ch includes other transcription factors like p73 and cancer-related microRNAs like miR-205.

38 e transcription factor c-Jun, a regulator of p73 and DeltaNp73, in both the cytoplasm and nucleus.

39 Prodigiosin induced the expression of p73 and disrupted its interaction with mutant p53, there

40 rstand genes and noncoding RNAs regulated by p73 and how they change during treatment regimens.

41 We found that mRNA expression levels of p73 and IGFBP3 are significantly lower in SGA children c

42 ), we measured the mRNA expression levels of p73 and IGFBP3 in a group of SGA children.

43 DeltaNp63alpha with a concurrent increase in p73 and its downstream target p21.

44 53-mutant cells, disrupts the interaction of p73 and mutant-p53, thereby releasing p73 from sequestra

45 ll-known tumour-related genes (that is, p53, p73 and p21) and survival rates of patients has been obs

46 activity, but forms a trimeric complex with p73 and p53R273H to more strongly inhibit p73 function.

47 p73 and p63 are evolving members of the p53 tumor suppre

48 n chromatin immunoprecipitation studies both p73 and p63 directly associated with the miR-200b/a/429

49 nomas in The Cancer Genome Atlas showed that p73 and p63 expression is significantly correlated with

50 predicted by the analysis to be regulated by p73 and p63, we found that p53/p63/p73 family binding si

51 unctions of other members of the p53 family, p73 and p63.

52 is through the transcriptional activation of p73 and perhaps other proapoptotic target genes.

53 ibit members of the p53 protein family, p53, p73 and possibly p63.

54 in immunoprecipitation (ChIP) and found that p73 and PTEN were associated with the PUMA promoter afte

55 d an increased expression in the presence of p73 and PTEN.

56 led that prodigiosin increased the levels of p73 and reduced levels of the oncogenic N-terminally tru

57 target of p73, the mutual regulation between p73 and RNPC1 constitutes a novel feed-forward loop, whi

58 analysis of the Noxa promoter revealed that p73 and Sp1-like factors, Sp1 and KLF6, played key roles

59 n, were increased markedly upon knockdown of p73 and TAp73 but little if any by DeltaNp73.

60 p53 pathway in cancer cells by upregulating p73 and targeting mutant p53/p73 interaction there.

61 ion of several p53 family members (p53, p63, p73) and a correlation between the levels of p53 family

62 s genome-wide redistribution of the cREL/p63/p73, and AP-1 interactome, to diminish TAp73 tumor suppr

63 p53, TA-p73, and p300 binding and Foxo3 expression decrease duri

64 However, different pathways regulate p53 and p73, and p73 is not mutated in human tumors.

65 ulated tumor-suppressor proteins (p27, FOXO, p73, and prostate apoptosis response-4 [PAR-4]) and inhi

66 p27T187A KI activated an E2F1-p73-apoptosis axis in DKO prostate tumorigenesis, slowed

67 ppressor gene p53 and its family members p63/p73 are critical determinants of tumorigenesis.

68 is a mammalian tumor suppressor and p63 and p73 are critical for development.

69 hree p53 gene family paralogs, p53, p63, and p73 are distinct genes.

70 he acidic transactivation domain) of p63 and p73 are frequently overexpressed in cancer and act prima

71 anscription factors, including p53, p63, and p73, are critical for many physiological processes, incl

72 on the intricate GH/IGF pathway, suggesting p73 as a good biomarker of the clinical risk for SGA chi

73 We report that Aurora-A phosphorylation of p73 at serine235 abrogates its transactivation function

74 Furthermore, BITC-induced p53 and p73 axes converge on tumor-suppressor LKB1 which is tran

75 p53 and TA-p73 bind a Foxo3 p53 response element (p53RE) and mainta

76 Both mutant p53 and p73 bind MDM2 well, whereas p63 binds much more weakly.

77 notype-including a conformational shift, p63/p73 binding and the ability to promote invasion.

78 In addition, multiple determinants of p73 binding, activity, and function were evident, and we

79 ain of mutant p53 is not required for p63 or p73 binding; indeed, mutations within this region lead t

80 A damage induced by bile acid exposure, only p73 (but not p53 and p63) is selectively activated in a

81 rve as a nuclear cofactor with DeltaNp63 and p73, but the functional role of YAP and their potential

82 Like p73, but unlike p53, p63 requires a second helix (H2) to

83 to characterize the potential regulation of p73 by HDACs and found that histone deacetylase 1 (HDAC1

84 ression changes due to inhibition of p63 and p73 by mutant p53 at their target gene promoters.

85 Moreover, we found that p73 can be degraded by both 20 S and 26 S proteasomes.

86 the p53 family as a whole, including p63 and p73, collaborate in controlling autophagy to support tum

87 Moreover, our results suggest that p73 compensates for loss of p53 and that targeting Mdm2

88 Tumor suppressors p53, p63 and p73 comprise a family of stress-responsive transcription

89 ant-negative variant of the tumor-suppressor p73, confers cancer cells with enhanced stem-like proper

90 Sequence variations in the RE elicit a p73 conformational response that might explain target ge

91 antly by p53, the p53 family members p63 and p73 contribute to activation of this autophagy gene netw

92 entify a microRNA-dependent mechanism of p63/p73 crosstalk that regulates p53-independent survival of

93 the high-resolution crystal structure of the p73 DBD as well as its complex with the ankyrin repeat a

94 We report two structures of the p73 DBD bound as a tetramer to 20-bp full-site REs based

95 We describe two main phenotypic variants of p73 deficiency in the brain, a severe one characterized

96 apitulates bile acid exposure, we found that p73 deficiency is associated with increased DNA damage.

97 press p73 and are particularly vulnerable to p73 deficiency.

98 Both variants display the core triad of p73 deficiency: cortical hypoplasia, hippocampal malform

99 p53-dependent and TA-p73-dependent activation of Foxo3 was also observed in m

100 nd that glutaminase 2 (GLS2), a modulator of p73-dependent antioxidant defense, is also involved in P

101 tivates the tyrosine kinase c-Abl to trigger p73-dependent apoptosis in mammary epithelial cells.

102 re therefore under investigation to activate p73-dependent apoptosis in p53-deficient cancer cells.

103 ivated in response to DNA damage and induces p73-dependent apoptosis.

104 upon DNA damage, leading to activation of a p73-dependent apoptotic response.

105 ulates p73 expression via mRNA stability and p73-dependent biological function in ROS production and

106 At therapeutic doses, NSC59984 induces p73-dependent cell death in cancer cells with minimal ge

107 Chemotherapy caused p63/p73-dependent induction of this microRNA, thereby limiti

108 ug adriamycin (doxorubicin) induces A2B in a p73-dependent manner and, in combination with an A2B ago

109 associated colon tumor xenograft growth in a p73-dependent manner in vivo.

110 be then employed for GSH synthesis, thus the p73-dependent metabolic switch enables potential respons

111 Signaling pathways including PKC- and p53/p73-dependent pathways are also common to melanocytes an

112 Importantly, we show that p73-dependent stimulation of A2B signalling markedly enh

113 It is thought to antagonize p53-, p63-, and p73-dependent translation, thus blocking their tumor sup

114 apoptosis induced by inhibition of Mdm2 was p73-dependent.

115 by determining the crystal structures of the p73 DNA-binding domain (DBD) in complex with full-site R

116 ts establish the quaternary structure of the p73 DNA-binding domain required as a scaffold to promote

117 e determined the first crystal structures of p73 DNA-binding domain tetramer bound to response elemen

118 zero and one base-pair spacers show compact p73 DNA-binding domain tetramers with large tetramerizat

119 ize knowledge on E2F1 and its interplay with p73/DNp73 and miR-205 in cancer drug responses, we deriv

120 -205, can be mediated by an imbalance in the p73/DNp73 ratio or by dysregulation of other cancer-rela

121 oherent feedforward loops that involve E2F1, p73/DNp73, and miR-205.

122 However, at molecular level p73 does not directly regulate serine metabolic enzymes,

123 phomas, and both the incidence and degree of p73 downregulation in these tumors correlated with their

124 gnificantly, the DNA-binding domain (DBD) of p73 escapes viral oncoproteins and displays an enhanced

125 -malignant B cells demonstrates that loss of p73 exacerbates the chromosome breaks and fusions observ

126 he p53-related transcription factors p63 and p73 exhibit distinct functions-p73 mediates chemosensiti

127 However, the MDM2-binding domain of p73 exhibits markedly stronger conservation suggesting n

128 ion can be used as an adjuvant treatment for p73-expressing medulloblastoma.

129 showed that loss of PCBP2 leads to decreased p73 expression and, subsequently, increased ROS producti

130 Mechanistically, BITC induces p73 expression in p53-mutant cells, disrupts the interac

131 ctively), whereas predefined analysis by p63/p73 expression status (n = 61), p53 and PIK3CA mutation

132 ether, our data suggest that PCBP2 regulates p73 expression via mRNA stability and p73-dependent biol

133 Consistent with this, p73 expression was frequently downregulated in a large c

134 hysiological significance of RNPC1-regulated p73 expression, we showed that the loss of RNPC1 in p53-

135 tion between serine biosynthetic pathway and p73 expression.

136 This pipeline nominated TFs of the p53/p63/p73 family as candidate drivers of miRNA overexpression.

137 ulated by p73 and p63, we found that p53/p63/p73 family binding sites modulate promoter activity of m

138 on of miRNAs whose promoters contain p53/p63/p73 family binding sites.

139 and dysfunction of tumor suppressor TP53/p63/p73 family transcription factors are key events in cance

140 t a subset of p63-regulated microRNAs target p73 for inhibition.

141 ionalizes previous observations that p63 and p73 form mixed tetramers, and the kinetic data reveal th

142 ion of p73 and mutant-p53, thereby releasing p73 from sequestration and allowing it to be transcripti

143 ly, we established a correlation between low p73 function and high IGF1R/CD133/Nanog/Oct4 levels in m

144 rent isoforms and regulation of p53, p63 and p73 function in the cell cycle.

145 Loss of p73 function in the ependyma may thus be one determining

146 th p73 and p53R273H to more strongly inhibit p73 function.

147 2 is a combined effect of inhibiting p53 and p73 functions.

148 nse rate (RR) and response prediction by p63/p73 gene expression.

149 A single p53/p63/p73 gene is in invertebrates and required for maintenanc

150 The p73 gene, a homologue of the p53 tumor suppressor, is ex

151 rate p53 gene and at least one ancestral p63/p73 gene.

152 Selected alleles of SNPs in p63 and p73 genes were enriched in IVF patients.

153 Here, we define the p73 genomic binding profile and demonstrate its modulati

154 For example, the mutant S139F in p73 has higher transactivation potential towards selecte

155 The p53 family member, p73, has been characterized as a tumor suppressor and fu

156 p53 and the transactivating p73 isoform (TA-p73) have hepatic-specific functions in development and

157 some of which, such as the tumor suppressor p73, have also been implicated in genomic instability.

158 kinetic data reveal the dissociation of the p73 homotetramers as the rate-limiting step for heterote

159 We show overexpression of p73 in a proportion of non-WNT medulloblastoma.

160 Mdm2 coprecipitates with p73 in activated T cells, and apoptosis induced by inhib

161 Elevated cytoplasmic p73 in Aurora-A overexpressing primary human tumors corr

162 utant p53s coaggregate with WT p53, p63, and p73 in cancer cell lines.

163 d found to be transcriptionally regulated by p73 in DNA damage conditions.

164 have demonstrated the involvement of p63 and p73 in female reproduction and their roles in egg format

165 Here, the role of p63 and p73 in human reproduction was investigated.

166 r strategies that involve the stimulation of p73 in order to efficiently restore tumor suppression.

167 cally relevant pathway to selectively induce p73 in p53-null cells.

168 is transcriptionally upregulated by p53 and p73 in p53-wild-type and p53-mutant cells respectively;

169 These findings implicate p73 in regulation of cancer metabolism and suggest that

170 up-regulation of the p53 gene family member p73 in response to DNA damage.

171 However, the role of p73 in the male germ line is unknown.

172 Due to the role of p73 in tumor suppression and neural development, its exp

173 6 and S100B to homologous domains of p63 and p73 in vitro by fluorescence anisotropy, analytical ultr

174 and apoptosis (p63) and spindle checkpoint (p73) in female mice.

175 ned whether PTEN would interact and regulate p73 independent of p53.

176 how that Salvador allows RASSF1A to modulate p73 independently of the hippo pathway.

177 However, how p63 and p73 interact functionally and govern the balance between

178 by upregulating p73 and targeting mutant p53/p73 interaction there.

179 The disruption of mutant p53/p73 interaction was specific to prodigiosin and not rela

180 to p53R175H but enhances the weaker p53R273H/p73 interaction.

181 potential role of MDM2 in the mutant p53/p63/p73 interactions.

182 utants trapped only small amounts of p63 and p73 into their p53 aggregates.

183 p73 is a member of the p53 protein family.

184 The loop in p73 is changed by a two-residue insertion that also indu

185 p73 is expressed as TA and DeltaN isoforms, both of whic

186 spontaneous tumors, the expression status of p73 is linked to the sensitivity of tumor cells to chemo

187 Given that p73 is lost or silenced in human B-cell lymphomas, the M

188 Functionally, p73 is more sensitive to spacer length than p53, with on

189 a high rate in human cancers, its homologue p73 is not mutated but is often overexpressed, suggestin

190 different pathways regulate p53 and p73, and p73 is not mutated in human tumors.

191 In contrast, p53 family member p73 is rarely mutated in colorectal cancer and p73 activ

192 While p73 is rarely mutated in spontaneous tumors, the express

193 ich element in the 3' untranslated region of p73 is recognized by and responsive to RNPC1.

194 Unlike p53, however, p73 is seldom mutated in cancer, making it an attractive

195 p73 Is thus involved in a variety of CNS activities rang

196 the p53 family, p53 and the transactivating p73 isoform (TA-p73) have hepatic-specific functions in

197 In contrast, loss of the oncogenic p73 isoform DeltaNp73 leads to reduced blood vessel form

198 738-1753) identify the p53 family member and p73 isoform TAp73 as a crucial factor causing glutamine

199 1300-1312) reveal the p53 family member and p73 isoform TAp73 as a transcription factor dictating th

200 rate that IGFBP3 is a direct TAp73alpha (the p73 isoform that contains the trans-activation domain) t

201 TAp73 is a p73 isoform with a potent transcriptional activation dom

202 and increased expression of transactivating p73 isoforms (TAp73).

203 ressed by p63, was activated by proapoptotic p73 isoforms in both normal cells and tumor cells in viv

204 A complex pattern of expression of p73 isoforms makes it difficult to unambiguously interpr

205 analyses revealed that expression of p63 and p73, key components known to arrest the cell cycle, was

206 Accordingly, p73 knockdown or DeltaNp73 overexpression suppressed pro

207 Total and N-terminal isoform selective p73 knockout mice show a variety of central nervous syst

208 In parallel, primary cortical neurons from p73 knockout mice showed a reduction in neurite outgrowt

209 he central and peripheral nervous systems of p73 knockout mice.

210 contributes to the neurological phenotype of p73 knockout mice.

211 xplanation for the diverse phenotypes of the p73 knockout mice.

212 Studies with p63- and p73-knockout mice have demonstrated the involvement of p

213 t E14.5, the incipient cortical plate of the p73 KO brains showed a reduced width.

214 studied the development of the neocortex in p73 KO mice from early embryonic life into advanced age

215 at deletion of the DeltaN isoforms of p63 or p73 leads to metabolic reprogramming and regression of p

216 ognized crosstalk between BITC, p53/LKB1 and p73/LKB1 axes in breast tumor growth-inhibition.

217 ping and expression profiling suggested that p73 loss allowed increased maturation of malignant B cel

218 In summary, Mdm2 overexpression and p73 loss cooperate in genomic instability and tumor deve

219 Specifically, p73 loss decreased nodal disease and increased widesprea

220 Here we have shown that p73 loss does not substantially affect disease onset and

221 ells and tumors with Mdm2 overexpression and p73 loss exhibit increased genomic instability as compar

222 xpressing phosphor-mimetic mutant (S235D) of p73 manifest altered growth properties, resistance to ci

223 Expression patterns of p63, p73, Mdm2, Mdm4, and Yy1 did not follow that of p53.

224 e UV and oxaliplatin-induced upregulation of p73 mediated by the transcription factor Egr1, but not t

225 MST2/LATS pathway, which is required for YAP/p73-mediated apoptosis, and negatively affected the acti

226 ge and inefficient DNA repair triggering p63/p73-mediated apoptosis.

227 to stimulate programmed cell death involving p73-mediated engagement of adenosine signalling.

228 ctors p63 and p73 exhibit distinct functions-p73 mediates chemosensitivity while p63 promotes prolife

229 ogical effects of Mdm2 loss, indicating that p73 mediates the consequences of Mdm2 deletion.

230 B-cell lymphomas from Mdm2(Tg);p73(+/-) mice retain the remaining p73 allele, exhibit e

231 Emu-myc-driven B cell lymphomagenesis, while p73 modulated tumor dissemination and extranodal growth.

232 nced in human B-cell lymphomas, the Mdm2(Tg);p73(+/-) mouse serves as a model for human disease and m

233 n compared with controls and, in particular, p73 mRNA expression is significantly lower in SGA childr

234 Here, we found that p73 mRNA stability is regulated by RNPC1, an RNA binding

235 We also showed that PCBP2 is necessary for p73 mRNA stability via the CU-rich elements in p73 3'-UT

236 erved with peptides derived from the p63 and p73 N-terminal transactivation domains.

237 tonomous mechanism involving inhibition of a p73/NF-Y complex that represses PDGFRb expression in p53

238 morphological and functional impairments in p73 null cells can be rescued by p75(NTR) re-expression.

239 p73 null mice also have impairments in the peripheral ne

240 Rapamycin selectively increased p73 occupancy at a subset of its binding sites.

241 Furthermore, we showed that knockdown of p73 or TAp73 in MCF10A cells led to a marked increase in

242 We also found that upon knockdown of p73 or TAp73, but not DeltaNp73, MCF10A cells underwent

243 set of the population have inherently weaker p73/p53 activation due to inefficient signaling through

244 d biochemical studies have demonstrated that p73, p63 and p53 recognize DNA with identical amino acid

245 transactivation potential nearly equally in p73, p63 and p53.

246 ein family, its three transcription factors (p73, p63, and p53) each trigger a gene expression patter

247 Here, we showed that upon knockdown of p73, particularly TAp73 but not DeltaNp73, MCF10A cells

248 lation of apoptosis by Gene 33 via the c-Abl/p73 pathway.

249 The p53 and p73 pathways role in metabolic adaptation, the effects o

250 p73 plays a critical role in a range of cellular metabol

251 Collectively our studies demonstrate that p73 plays an important role in the regulation of DNA dam

252 The transcription factor p73 plays critical roles during development and tumorige

253 anscription factors--comprising p53, p63 and p73--plays an important role in tumor prevention and dev

254 To address how p73 possesses these opposing functions, we developed thr

255 Interestingly, p73 produces two classes of proteins with opposing funct

256 The activated p73 protein induces DNA damage repair.

257 al cells to bile acids in acidic conditions, p73 protein plays the predominant role in the DNA damage

258 anscripts, which in TP73 encodes a truncated p73 protein with oncogenic function and in TERT encodes

259 irus-transduced cell lines stably expressing p73, PTEN, or both p73/PTEN, we found that the p73/PTEN

260 Both overexpressed and endogenous p73-PTEN interactions were determined to be the stronges

261 Thus, a p73-PTEN protein complex is engaged to induce apoptosis

262 3, PTEN, or both p73/PTEN, we found that the p73/PTEN cells were more sensitive to genotoxic stress a

263 tion in the nucleus and complex formation of p73/PTEN were observed after DNA damage.

264 l lines stably expressing p73, PTEN, or both p73/PTEN, we found that the p73/PTEN cells were more sen

265 The structural similarity between p63 and p73 rationalizes previous observations that p63 and p73

266 noma cells exhibit hypermethylation within a p73 regulatory region, which includes the binding site f

267 Therefore, p73 represents a therapeutic target, and there is a crit

268 RNAi-mediated attenuation of p73 rescued the transcriptional and biological effects o

269 embers, Tp63 and Tp73 (also known as p63 and p73, respectively).

270 cell death induced by Mdm2 inhibition, and a p73-responsive element in intron 1 of Bim was characteri

271 3 restoration is known to target CRCSCs, but p73 restoration in CRCSCs has not been examined.

272 Knockout of all three members, p53, p63, and p73, shows that the p53 family is essential for mesendod

273 We generated an mTOR-p73 signature that is enriched for p73 target genes and

274 t p53 needs to be targeted in the context of p73 stimulation to allow efficient restoration of the p5

275 tion-domain-bearing (TA) isoforms of p63 and p73 structurally and functionally resemble p53, whereas

276 The p73 structure exhibits the same conserved architecture a

277 In these tumors, p73 sustains cell growth and proliferation via regulatio

278 Further, Bim was identified as a p73 target gene required for cell death induced by Mdm2

279 d an mTOR-p73 signature that is enriched for p73 target genes and miRNAs that are involved in mesench

280 es cyclin A and Cdk1 and upregulation of p63/p73 target genes such as Bax and Noxa.

281 We found that another p73 target, BAX, had an increased expression in the pres

282 ow inflammatory gene signatures and cREL/p63/p73 targets are comodulated genome wide is unclear.

283 xpression of inflammatory genes and TP53/p63/p73 targets were detected in the PanCancer 12 project, r

284 6 and S100B proteins bound different p63 and p73 tetramerization domain variants and naturally occurr

285 p73, the closely related p53 family member, can regulate

286 Due to the fact that RNPC1 is a target of p73, the mutual regulation between p73 and RNPC1 constit

287 tion of the liver, the binding of p53 and TA-p73, the recruitment of acetyltransferase p300, and the

288 for full apoptotic activity and to activate p73, this effect does not require a direct interaction o

289 the interaction partner of YAP from TEAD to p73 through YAP phosphorylation at Thr77.

290 p73, through GLS-2, favors conversion of glutamine in gl

291 forward mechanism, LKB1 tethers with p53 and p73 to get recruited to p53-responsive promoters.

292 /glycine-deprivation, supporting the role of p73 to help cancer cells under metabolic stress.

293 s by targeting GOF-mutant p53 and stimulates p73 to restore the p53 pathway signaling.

294 We report here the ability of p73 to upregulate the expression of the A2B receptor, a

295 ion, which includes the binding site for the p73 transcriptional repressor ZEB1, leading to the abrog

296 The transcription factor p73 triggers developmental pathways and overlaps stress-

297 TAp63, but not DeltaNp63, p53 or p73, upregulates CCDC3 expression by directly binding to

298 o further understand the variant features of p73, we solved the high-resolution crystal structure of

299 uch as R175H) show strong binding to p63 and p73, whereas p53 mutants that only mildly affect the con

300 ance between TEAD/YAP-dependent necrosis and p73/YAP-dependent apoptosis by shifting the interaction