ライフサイエンスコーパス: p73

1 lead to apoptosis via activation of p63 and p73.

2 uppress 2 other p53 family proteins, p63 and p73.

3 optosis by upregulating the tumor suppressor p73.

4 xhibiting much faster exchange kinetics than p73.

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

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

7 to microRNA-mediated feedback inhibition of p73.

8 ates, expression of endogenous and exogenous p73.

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

10 ion of the transcriptional activities of p63/p73.

11 tified multiple DNA repair genes affected by p73.

12 otes the proteasome-dependent degradation of p73.

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

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

15 3 mRNA stability via the CU-rich elements in p73 3'-UTR.

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

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

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

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

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

21 3 is rarely mutated in colorectal cancer and p73 activation elicits p53-like tumor suppression.

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

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

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

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

26 3 by p53R175H, but enhance the inhibition of p73 activity by p53R175H and R273H.

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

28 lysis indicates that the p53 family protein, p73, affects Th1 differentiation.

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

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

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

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

33 Our data shed light on the relevance of p73 alternative splicing and show that the full-length C

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

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

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

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

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

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

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

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

42 53-mutant cells, disrupts the interaction of p73 and mutant-p53, thereby releasing p73 from sequestra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Importantly, the levels of p73 are elevated in HPV-positive cells and its knockdown

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

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

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

71 Our results thus identify p73 as a negative regulator of the Th1 immune response,

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

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

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

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

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

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

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

79 p73 binds within, or upstream of, and modulates the expr

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

81 nhibited DNA binding by p53 and homologs p63/p73, but did not affect E2F1, TCF1, and c-Myc.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 press p73 and are particularly vulnerable to p73 deficiency.

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

100 mouse experimental autoimmune encephalitis, p73-deficient mice have increased IFNgamma production an

101 by using mutant p53-R270H knockin and TAp63/p73-deficient mouse models.

102 l of inflammatory bowel disease, transfer of p73-deficient naive CD4(+) T cells increases Th1 respons

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 -205, can be mediated by an imbalance in the p73/DNp73 ratio or by dysregulation of other cancer-rela

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

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

126 of the Th1 immune response, suggesting that p73 dysregulation may contribute to susceptibility to au

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

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

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

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

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

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

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

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

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

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

137 tion between serine biosynthetic pathway and p73 expression.

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

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

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

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

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

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

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

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

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

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

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

149 2 is a combined effect of inhibiting p53 and p73 functions.

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

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

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

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

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

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

156 The p53 family member p73 has a complex gene structure, including alternative

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

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

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

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

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

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

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

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

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

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

167 ssion of E2F1, a TopBP1-binding partner, and p73 in HPV-positive cells in contrast to its effects in

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

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

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

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

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

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

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

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

176 6 and S100B to homologous domains of p63 and p73 in vitro by fluorescence anisotropy, analytical ultr

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

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

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

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

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

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

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

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

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

186 p73 is a member of the p53 protein family.

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

188 and show that the full-length C terminus of p73 is essential for hippocampal development.

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

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

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

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

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

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

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

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

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

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

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

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

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

202 738-1753) identify the p53 family member and p73 isoform TAp73 as a crucial factor causing glutamine

203 1300-1312) reveal the p53 family member and p73 isoform TAp73 as a transcription factor dictating th

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

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

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

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

208 Accordingly, p73 knockdown or DeltaNp73 overexpression suppressed pro

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

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

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

212 contributes to the neurological phenotype of p73 knockout mice.

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

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

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

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

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

218 This demonstrates that p73, like p63 and p53, is an important regulator of the

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

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

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

227 racellular domain (NICD) and antagonized p63/p73-mediated repression of HES1 and ECM1.

228 examined whether mutant p53 antagonizes p63/p73-mediated tumor suppression in vivo by using mutant p

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

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

231 mutant p53-R270H shortened the life span of p73 (+/-) mice and subjected TAp63 (+/-) or p73 (+/-) mi

232 p73 (+/-) mice and subjected TAp63 (+/-) or p73 (+/-) mice to T lymphoblastic lymphomas (TLBLs).

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

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

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

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

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

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

239 ifferentiated under Th1 conditions in vitro, p73 negatively regulates IFNgamma production.

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

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

242 p73 null mice also have impairments in the peripheral ne

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

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

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

246 rexpressed in TAp63 (+/-) ;p53 (R270H/-) and p73 (+/-) ;p53 (R270H/-) TLBLs, suggesting that normal f

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

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

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

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

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

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

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

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

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

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

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

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

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

260 The activated p73 protein induces DNA damage repair.

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

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

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

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

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

266 3, PTEN, or both p73/PTEN, we found that the p73/PTEN cells were more sensitive to genotoxic stress a

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

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

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

270 nism by which GOF mutant p53 hijacks the p63/p73-regulated transcriptional program via the Notch1 pat

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

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

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

274 3 restoration is known to target CRCSCs, but p73 restoration in CRCSCs has not been examined.

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

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

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

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

279 The p73 structure exhibits the same conserved architecture a

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

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

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

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

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

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

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

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

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 The transcription factor p73 triggers developmental pathways and overlaps stress-

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

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

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

299 inhibitors suppresses expression of E2F1 and p73 without interfering with ATR signaling.

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