ライフサイエンスコーパス: p53 protein

1 nduced up-regulation of the tumor suppressor p53 protein.

2 ys, we demonstrate that SIRT1-Delta2/9 binds p53 protein.

3 ed to the inhibition of reprogramming by the p53 protein.

4 ssion of a transcriptionally inactive mutant p53 protein.

5 solely through controlling the stability of p53 protein.

6 an arginine or proline at position 72 of the p53 protein.

7 t gene to mediate these two functions of the p53 protein.

8 use the viral E6 oncoprotein inactivates the p53 protein.

9 ed levels of 8-hydroxy-2'-deoxyguanosine and p53 protein.

10 a-amanitin leads to accumulation of cellular p53 protein.

11 of the respective genes by the overexpressed p53 protein.

12 s and the accompanying acidosis, not loss of p53 protein.

13 etylation, resulting in stabilization of the p53 protein.

14 d increase in apoptosis and up-regulation of p53 protein.

15 EBP induction of cell growth and increase in p53 protein.

16 mutations resulting in a full-length mutant p53 protein.

17 Pla2g16 is a downstream target of the mutant p53 protein.

18 ne that result in the expression of a mutant p53 protein.

19 modulates both the wild-type and the mutant p53 proteins.

20 affecting the ubiquitylation or stability of p53 proteins.

21 expressed similar levels of P16, SMAD4, and P53 proteins.

22 tations, leading to the expression of mutant p53 proteins.

23 N-terminal Apoptosis-stimulating of p53 protein 2 (ASPP2) mediates RAS-induced senescence an

24 r negative regulator of the tumor suppressor p53 protein, a protein that plays a crucial role in main

25 The p53 protein, a transcription factor of key importance in

26 anocomposite) was developed for detection of p53 protein, a well-known tumor suppressor.

27 nic fibroblasts (mef's), leading to enhanced p53 protein accumulation and p53-dependent senescence.

28 All but the p53-null cells displayed p53 protein accumulation in a time-dependent manner on n

29 Molecular markers, including p53 protein accumulation, p53-activated genes, and BRCA1

30 M/ATR-dependent p53 phosphorylation or total p53 protein accumulation.

31 direct control of Flt1 expression by ER and p53 proteins acting as sequence-specific transcription f

32 ring is overwhelmed by de novo expression of p53 protein after DNA damage induced by genotoxic stress

33 Optimal induction of p53 protein after DNA damage requires RPL26-mediated inc

34 sulted from a decreased stabilization of the p53 protein after stress.

35 ncer cells with cancer stem cell properties, p53 protein aggregation is associated with p53 inactivat

36 The function of p53 protein, also known as "genome guardian", might be i

37 We have previously reported that p53 protein, although a well-known tumor suppressor, can

38 ubunit reduces the steady-state level of the p53 protein, although there is no effect on the p53 prot

39 GA downregulated overexpressed mutant p53 protein (an oncogene) and upregulated wild-type (wt)

40 erved only in tumors with constitutively low p53 protein and accumulation upon cisplatin treatment.

41 ed cells with 9AA resulted in an increase in p53 protein and activation of p53 transcription activity

42 destabilises Mdm2 and causes accumulation of p53 protein and activation of p53.

43 In this study, we showed that both p53 protein and activity levels in melanoma cells were s

44 s response by orchestrating up-regulation of p53 protein and consequently promoting cell-cycle delay.

45 lation of Sox2 expression, and demethylating p53 protein and consequently, modulating its target gene

46 Activated B cell clones exhibit elevated p53 protein and elevated mRNA/protein of proapoptotic mo

47 MAML1 increases the half-life of p53 protein and enhances its phosphorylation/acetylation

48 re is a great deal of cross-talk between the p53 protein and epigenetic programs.

49 epigenetic protein modifications act on the p53 protein and its splice variants in stem and progenit

50 ovide unique insights into the regulation of p53 protein and may contribute to the understanding of t

51 is, mother cells transmit DNA damage-induced p53 protein and mitogen-induced cyclin D1 (CCND1) mRNA t

52 te that the HDAC8 protein interacts with the p53 protein and modulates p53 activity via deacetylation

53 izing radiation (IR) and measuring levels of p53 protein and one of its transcriptional targets, the

54 ion by inhibiting Mdm2 resulted in sustained p53 protein and prevented antigen-specific T cell prolif

55 DINO bound to p53 protein and promoted its stabilization, mediating a

56 ation of Mdm2 by siRNA led to an increase in p53 protein and repression of Cdc25C gene expression.

57 Ybox1 binds both the Trp53 promoter and the p53 protein and that expression of Trp53 is significantl

58 f human epithelial cells: the degradation of p53 protein and the induction of telomerase.

59 tes led to reduced MDM2 levels and increased p53 protein and transcriptional activity, reduction in K

60 ulting in reduced levels of the E6-regulated p53 proteins and E7 oncoprotein itself.

61 rm of PA28gamma interacts with both MDM2 and p53 proteins and facilitates their physical interaction.

62 the relationship between wild-type or mutant p53 proteins and the target response elements.

63 tial effects on the activity of the MDM2 and p53 proteins and to associate with altered risk for the

64 decreased expression of wild-type and mutant p53 proteins and transcripts.

65 nzymes (OGG-1, Neil 1) and check point (p21, p53) proteins and avoid the mtDNA mutations.

66 half of human tumors harbor mutant forms of p53 protein, approaches aimed at disrupting the patholog

67 shown to affect the biochemical functions of p53 protein are the exon 4 Arg72pro, Intron 3 16bp Del/I

68 Such neomorphic p53 proteins are capable of dramatically altering tumor

69 ith this, the levels of wild-type and mutant p53 proteins are decreased upon treatment with HDAC inhi

70 both sets of models, the human or humanized p53 proteins are functional as evidenced by the transcri

71 Accumulated mutant p53 proteins are known to actively contribute to tumor d

72 d with covalently immobilized HaloTag fusion p53 protein as solid supports for the selective capture

73 -immortalized cells expressed high levels of p53 protein as well as two p53-regulated proteins, p21 a

74 ssion, the accumulation and stabilization of p53 protein, as well as the activation of the apoptotic

75 The apoptosis stimulating p53 proteins, ASPP1 and ASPP2, are the first two common

76 These drugs reduced the basal levels of p53 protein at nanomolar concentrations in a dose-, time

77 hibition by MG132 increases the occupancy of p53 protein at p53-responsive p21(waf1) promoter.

78 ChIP analysis revealed that several mutant p53 proteins bind the Pla2g16 promoter at E26 transforma

79 ed in susceptible mouse strains, in the Daxx-p53 protein-binding region.

80 e the first demonstration that (a) wild-type p53 protein binds to a response element within the EpCAM

81 We also found that p53 protein binds to and activates the promoter of the R

82 CypD causes strong aggregation of wild-type p53 protein (both full-length and isolated DNA-binding d

83 embryo fibroblasts, AMPK phosphorylates the p53 protein but does not activate any of the p53 respons

84 c + E7 cells is due not to the levels of the p53 protein but rather to unique properties of the Myc p

85 An shRNA-directed reduction in p53 protein by about 50% also results in extended cellul

86 In addition, upregulation of p53 protein by Nutlin-3 prevents SIRT6 reduction and DNA

87 ategies we demonstrate that hAda3 stabilizes p53 protein by promoting its acetylation.

88 EBPalpha and translational repression of the p53 protein by the CUGBP1-eukaryotic initiation factor 2

89 Indeed, this mutant p53 protein can be degraded by Mdm2 but fails to interac

90 The p53 protein can directly bind to a short 15-nucleotide s

91 get for mutation in human tumors, and mutant p53 proteins can actively contribute to tumorigenesis.

92 RNA-binding protein and a target gene of the p53 protein, can regulate p21 expression via mRNA stabil

93 function through the disruption of the MDM2-p53 protein complex is a promising strategy for the trea

94 The S100B-p53 protein complex was discovered in C8146A malignant m

95 p53 protein conformation is an important determinant of

96 ubiquitin receptor S5a/PSMD4/Rpn10 inhibits p53 protein degradation and results in the accumulation

97 NSC59984 induces mutant p53 protein degradation via MDM2 and the ubiquitin-prote

98 3 promoter-driven transcription activity and p53 protein degradation were comparable between wild-typ

99 key negative regulator of p53, and promotes p53 protein degradation.

100 ous multimerization domains from the GCN4 or p53 proteins, demonstrates that tetramers of Rta are suf

101 TAF promoter; the specific site required for p53 protein-DNA binding is located between -550 and -500

102 We found that the Tbx1 and p53 proteins do not interact directly but both occupy a

103 ion of label-free detection of intracellular p53 protein dynamics through a nanoscale surface plasmon

104 re, we show that Mysm1-deficiency results in p53 protein elevation in many hematopoietic cell types.

105 urn, inhibit the activity of the full-length p53 protein, establishing a novel negative feedback loop

106 Many mutant p53 proteins exert oncogenic gain-of-function (GOF) prop

107 Many mutant p53 proteins exert oncogenic gain-of-function (GOF) prop

108 Predicted sequences for human and clam p53 proteins exhibit conservation in key domains.

109 t in T24T and HCT116 cells without affecting p53 protein expression and activation.

110 R signaling resulted in early termination of p53 protein expression by decreasing p53 mRNA as well as

111 This suggests that p53 protein expression is differentially regulated depen

112 over, irrespective of the differences in the p53 protein expression profile, gammaIR-induced p53 acti

113 samples, immunohistochemistry evaluation of p53 protein expression revealed the presence of epiderma

114 Inhibition of p53 protein expression using small interfering RNA abrog

115 Consistent with this, p53 protein expression was up-regulated and had increase

116 on of p50 (p50-/-) impaired arsenite-induced p53 protein expression, which could be restored after re

117 iveness without affecting mutant full-length p53 protein expression.

118 f 27 cell lines that correlated with loss of p53 protein expression.

119 h1 promoter vicinity and also interacts with p53 protein, facilitating or increasing Notch1 signaling

120 few detailed studies of the entire extended p53 protein family have been reported, and none comprehe

121 is a transcription factor and member of the p53 protein family that expresses as a complex variety o

122 , are the first two common activators of the p53 protein family that selectively enable the latter to

123 PP2 interact with the DNA-binding domains of p53 protein family with dissociation constants, K(d), in

124 In the case of the p53 protein family, its three transcription factors (p73

125 eins that bind to and inhibit members of the p53 protein family, p53, p73 and possibly p63.

126 p73 is a member of the p53 protein family.

127 Although p53 protein function has been clearly linked to the cell

128 In tumours that harbour wild-type p53, p53 protein function is frequently disabled by the mouse

129 ter MI219 treatment, indicative of defective p53 protein function or defects in the apoptotic p53 net

130 tinct activators (i.e., the tumor suppressor p53 protein, glutamine-rich Sp1 and the oncoprotein c-Ju

131 nation and increases p53 levels by extending p53 protein half-life, whereas siRNA silencing of RPS27L

132 The aggregation of p53 protein has been discovered in different types of ca

133 dding acetyl groups to the C terminus of the p53 protein has been suggested to be required for its fu

134 The p53 protein has not only important tumor suppressor acti

135 This mutant p53 protein has, in most cases, lost wild-type transcrip

136 Recently, mutant p53 proteins have been shown to mediate metabolic change

137 Using this approach, dimethyl-histone H3 and p53 proteins have been synthesized and used to probe fun

138 s the nuclear factor-kappa B (NF-kappaB) and p53 proteins; however, the p53 activity is antagonized b

139 Mass spectrometry of GSH-modified p53 protein identified cysteines 124, 141, and 182, all

140 rved a 30- to 40-fold induction of wild-type p53 protein in 50 distinct human CLL specimens tested, w

141 to the expression of the full-length mutant p53 protein in cancer cells.

142 We also show that the conformation of mutant p53 protein in ESCs is stabilized to a WT conformation.

143 Expression of p53 protein in p53(-/-) cells suppressed basal and uroki

144 as indicated by the biphasic accumulation of p53 protein in the basal versus luminal layer.

145 en species, gammaH2AX DNA damage marker, and p53 protein in the hematopoietic progenitors.

146 s successfully applied for quantification of p53 protein in the human spiked serum samples and more i

147 terestingly, a significant proportion of the p53 protein in the Myc + E7-immortalized cells was local

148 istent DNA damage and sustained induction of p53 protein in the wild-type livers, and much less induc

149 Thus, promoting the removal of mutant p53 proteins in cancer cells may have therapeutic signif

150 ent of ribosomal biogenesis can activate the p53 protein independently of DNA damage.

151 fter mitosis, the transferred CCND1 mRNA and p53 protein induce variable expression of cyclin D1 and

152 However, p53 protein induced in this manner could transcriptional

153 M is capable of inducing the accumulation of p53 protein, inducing significant apoptotic cell death w

154 t molecular defects, including low or absent p53 protein induction after MDM2 inhibitor treatment or

155 subset of resistant blasts displayed robust p53 protein induction after MI219 treatment, indicative

156 The mechanisms by which the p53 protein inhibits the formation of iPSCs are largely

157 inal region (amino acid residues 296-393) of p53 protein interacts with PAI-1 mRNA.

158 The p53 protein is a key transcriptional factor regulating c

159 The p53 protein is a sequence-specific DNA-binding factor th

160 The p53 protein is a tumor suppressor protein that promotes

161 ical analysis showing > 50% cells expressing p53 protein is a useful surrogate and was able to strati

162 Rescuing the function of mutant p53 protein is an attractive cancer therapeutic strategy

163 The p53 protein is an important tumor suppressor that regula

164 The p53 protein is critical for multiple cellular functions

165 f of all human cancers, the tumor suppressor p53 protein is either lost or mutated, frequently result

166 Correct folding of the p53 protein is essential for these activities, and point

167 The full-length p53 protein is largely inactive in stem cells but, when

168 ted in normal cells, and thus, the wild-type p53 protein is nearly undetectable until stimulated thro

169 In addition, the sclerotomal accumulation of p53 protein is observed in transgenic embryos, suggestin

170 ghly conserved homologue for wild-type human p53 protein is rendered nonfunctional by cytoplasmic seq

171 TP53 (which encodes the p53 protein) is the most frequently mutated gene among a

172 TP53 (which encodes p53 protein) is the most frequently mutated gene among a

173 Antibodies specific to p53 protein isoforms have proven difficult to develop, t

174 a new mechanism regarding the making of the p53 protein itself.

175 mechanism that involves stabilization of the p53 protein leading to increased p53 binding to the p21(

176 embryonic fibroblasts increased the level of p53 protein, leading to enhanced premature senescence in

177 2 in the p53-binding pocket and displace the p53 protein, leading to p53-mediated cell cycle exit and

178 rate is attributable to abnormally increased p53 protein level and activity in the absence of Redd1.

179 suppression of JNK1 by JNK1 siRNA increased p53 protein level and decreased PS1 expression.

180 rora B in cancer cells with WT p53 increased p53 protein level and expression of p53 target genes to

181 to the nucleus, where it binds and regulates p53 protein level and transcription activity.

182 results in a significantly decreased nuclear p53 protein level and transcriptional activity, enhanced

183 protein, although there is no effect on the p53 protein level in the absence of the ESSS subunit tha

184 The p53 protein level was also reduced to undetectable level

185 with the reduction of the RNAP LS level, the p53 protein level was greatly induced.

186 s revealed that in RNF2 knockdown cells, the p53 protein level was increased, the half-life of p53 wa

187 cells overexpressing RNF2 showed a decreased p53 protein level, a shorter p53 half-life and increased

188 bearing wild-type p53 by inducing a surge in p53 protein level.

189 p53 protein levels and activity are under a tight and co

190 Depletion of Trim39 significantly increased p53 protein levels and cell growth retardation in multip

191 soforms results in a significant increase in p53 protein levels and dramatically stimulates p53-depen

192 utes a positive feedback loop that increases p53 protein levels and enhances the transactivation of i

193 negative regulator of p53; LIF downregulates p53 protein levels and function in human colorectal canc

194 hosphorylation status of Mdm2 Ser394 governs p53 protein levels and functions in cells undergoing DNA

195 Overexpression of miR-504 decreases p53 protein levels and functions in cells, including p53

196 ys, these compounds were shown to upregulate p53 protein levels and p53 signaling and to cause p53-de

197 tly target the 3'UTR of TP53 to downregulate p53 protein levels and reduce the expression of genes th

198 of K-Ras, RalB, and sometimes RalA increases p53 protein levels and results in a p53-dependent up-reg

199 SIRT1-Delta2/9 maintains basal p53 protein levels and supports p53 function in response

200 We now demonstrate that p53 protein levels are increased in infected brains duri

201 ns have been implicated in the regulation of p53 protein levels as well as its DNA binding and transc

202 NMT1 to the RASSF1A promoter, fluctuation in p53 protein levels did not affect the rates of RASSF1A m

203 Notably, decreasing p53 protein levels enabled fibroblasts to give rise to i

204 lular stress response by regulating Mdm2 and p53 protein levels following severe DNA damage.

205 Despite heightened p53 protein levels in cells expressing certain E1B-55K m

206 cells rapidly assemble into tetramers before p53 protein levels increase.

207 dent manner: cjoc42 prevents the decrease in p53 protein levels normally associated with high amounts

208 that these immortal MECs select for reduced p53 protein levels through a proteasome-dependent mechan

209 y, we show that PTEN expression enhances mut-p53 protein levels via inhibition of mut-p53 degradation

210 by direct targeting of Myc, which sustained p53 protein levels via the Arf-Hdm2 pathway.

211 p53 protein levels were up-regulated independently of MM

212 p53 protein levels were upregulated at similar rates in

213 hanced phosphorylation at Ser(46), increased p53 protein levels, and induction of Noxa expression.

214 EC TUNEL staining, caspases 3, 8, and 9, and p53 protein levels, induced by anti-CD3 monoclonal antib

215 of a DNA-damaging agent further upregulated p53 protein levels, which led to apoptosis.

216 onse by controlling base excision repair and p53 protein levels.

217 es was attenuated, despite markedly elevated p53 protein levels.

218 or protein (p53) at serine 18, and increased p53 protein levels.

219 esulting in an approximately 50% decrease in p53 protein levels.

220 -type p53-harboring cancer cells by reducing p53 protein levels.

221 ding to Mdm2 repression followed by elevated p53 protein levels.

222 but not apoptosis; increased phosphorylated p53 protein levels; and expression of p53 target genes i

223 y enhancing gain-of-function mutant p53 (mut-p53) protein levels.

224 endogenously expressed or exogenously added p53 protein localizes to the nucleolus in detergent-perm

225 The p53 protein maintains stability of the genome through th

226 P53 genotyping with functional evaluation of p53 protein may contribute significantly to the precise

227 Certain mutant p53 proteins may exhibit a 'gain of oncogenic function'.

228 Intriguingly, p53 proteins mutated to prevent the interaction with CCT

229 Mutant p53 proteins (mutp53) often acquire oncogenic activities

230 Many mutant p53 proteins (mutp53s) exert oncogenic gain-of-function

231 The p53 protein not only enforces the stability of the genom

232 Mutant p53 protein often accumulates to very high levels in tum

233 Accordingly, the effect of different mutant p53 proteins on cancer cell metabolism is largely unknow

234 he absence of Cre, whereas B cells expressed p53 protein only in the presence of B cell-specific CD19

235 ion in HCT116 cells does not involve altered p53 protein or phosphorylation, and we show that LRH-1 i

236 provide evidence that cells lacking Ras and p53 proteins owe their proliferative properties to the u

237 us epidermal patches that stain positive for p53 protein (p53 immunopositive patches, PIPs), which ar

238 eleted additionally for the tumor suppressor p53 protein (p53).

239 0B)), wt p53 mRNA levels were unchanged, but p53 protein, phosphorylated p53, and p53 gene products (

240 The p53 protein plays a central role in the prevention of tu

241 It is well established that the p53 protein plays a crucial role in the control of tumor

242 The evolutionary appearance of p53 protein probably preceded its role in tumor suppress

243 Tumour-derived mutant p53 proteins promote invasion, in part, by enhancing Rab

244 mall-molecule inhibitors that block the MDM2-p53 protein-protein interaction (MDM2 inhibitors) are be

245 Structural analysis of both the MDM2-p53 protein-protein interaction and several small molecu

246 hibitors (MDM2 inhibitors) to block the MDM2-p53 protein-protein interaction has been pursued as a ne

247 he oncoprotein murine double minute 2 (MDM2)-p53 protein-protein interaction has long been considered

248 Inhibition of the MDM2-p53 protein-protein interaction is being actively pursue

249 he discovery of novel inhibitors of the MDM2-p53 protein-protein interaction.

250 yrim idine as a potent inhibitor of the MDM2-p53 protein-protein interaction.

251 selective piperidinone inhibitor of the MDM2-p53 protein-protein interaction.

252 etramerization domain may potentially affect p53 protein/protein interactions.

253 of p21 protein accumulation despite a normal p53 protein response.

254 re not functional in p53 absence, but mutant p53 proteins retain partial MET promoter suppression.

255 Mutant p53 protein(s) (mutp53) can acquire oncogenic properties

256 an increased abundance of the S. frugiperda P53 protein (SfP53) and phosphorylation of the histone v

257 he C terminus of beta-actin or NLSIII of the p53 protein, slide along DNA.

258 Purified p53 protein specifically binds to the PAI-1 mRNA 3'-un-t

259 Purified p53 protein specifically binds to the uPAR mRNA 3' untra

260 em plays a pivotal role in the regulation of p53 protein stability and activity.

261 n, both are capable of negatively regulating p53 protein stability and promoting the intracellular ub

262 PNR also increased p53 protein stability and specific activity as a transcr

263 Mechanistically, miR-542-3p increased p53 protein stability by weakening interactions between

264 We analyzed whether CK1 regulates p53 protein stability in unstressed conditions.

265 reases-whereas knockdown of ZFP871 increases-p53 protein stability through a proteasome-dependent deg

266 Pax3 reduced p53 protein stability, but had no effect on p53 mRNA lev

267 mulation detectable by immunohistochemistry; p53 protein status) are associated with bladder cancer p

268 ays, reduce the p53 levels via inhibition of p53 protein synthesis.

269 we established that PRMT5 knockdown prevents p53 protein synthesis.

270 n of p53K382me2 promotes the accumulation of p53 protein that occurs upon DNA damage, and this increa

271 s results in the expression of point-mutated p53 proteins that have both lost wild-type tumor suppres

272 Many cancers express mutant p53 proteins that have lost wild-type tumor suppressor a

273 code proteins that monitor DNA damage (e.g., p53), proteins that regulate the cell cycle (such as Rb)

274 ry of causing changes in the genome, and the p53 protein, the function of which is to protect against

275 first demonstration of effective full-length p53 protein therapy in vivo.

276 nal antibody (mAb) 3E10 Fv antibody-mediated p53 protein therapy, an Fv-p53 fusion protein produced i

277 c trioxide decreases the stability of mutant p53 protein through a proteasomal pathway, and blockage

278 This results in the stabilization of p53 protein through abrogation of MDM2-mediated p53 ubiq

279 slowed down the turnover of both Poleta and p53 proteins through destabilizing their E3 ligase murin

280 ng domain (p53DBD) and full-length wild-type p53 protein to a single p53 response element (p53RE) pla

281 vity of ectopically expressed wild-type (WT) p53 protein to that of a truncated mutant lacking the 24

282 enhanced UGT2B7 expression and recruited the p53 protein to the UGT2B7 p53RE in HepG2 cells.

283 a novel function of p50 in its regulation of p53 protein translation under stress conditions.

284 tified a novel function of p50 in modulating p53 protein translation via regulation of the miR-190/PH

285 Additionally, expression of the p53 protein triggered apoptosis in a subset of the Saos-

286 wn for the first time to be regulated by the p53 protein, TSC2, PTEN, and IGF-BP3, each of which nega

287 d expression of CDK inhibitors and decreased p53 protein turnover, which blocked their tumorigenic ca

288 es and some tumors have low levels of mutant p53 protein unless Mdm2 or p16(INK4A) are absent.

289 ough" drug led to restoration of full-length p53 protein, upregulation of p53 downstream transcripts,

290 Contrary to expectations, functional p53 protein was expressed in the thymus and multiple oth

291 p53 protein was increased in resting Mule-deficient mous

292 ed GSH or GSSG into the purified recombinant p53 protein was observed.

293 By overexpression of a dominant-negative p53 protein, we show that ABT-737-induced cellular senes

294 These factors stabilized mutant p53 protein which oftentimes contributed to exacerbated

295 deletion leads to a drastic stabilization of p53 protein, which can be attributed to a requirement of

296 in regulating the levels and activity of the p53 protein, which is a central tumor suppressor.

297 ) signal, IL-2 induced sustained increase in p53 protein, which prevented proliferative responses des

298 or-suppressor function onto mutant, inactive p53 proteins will prove to be more efficacious than trad

299 Treatment of purified p53 protein with anti-p53 antibody abolished p53 binding

300 Numerous cells accumulated p53 protein, without inducing apoptosis, but the product