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1 repress the transcriptional activity of the tumor suppressor protein p53.
2 be a specific inhibitor of signaling by the tumor suppressor protein p53.
3 g homology to the proline-rich domain of the tumor suppressor protein p53.
4 to activation of a checkpoint involving the tumor suppressor protein p53.
5 lly deubiquitinates and hence stabilizes the tumor suppressor protein p53.
6 ant regulator of the proapoptotic BAX is the tumor suppressor protein p53.
7 at that this AR activity is repressed by the tumor suppressor protein p53.
8 Mdm2 is a critical negative regulator of the tumor suppressor protein p53.
9 oter DNA sequence in a complex stabilized by tumor suppressor protein p53.
10 ceptor is transcriptionally regulated by the tumor suppressor protein p53.
11 is through its interaction with the cellular tumor suppressor protein p53.
12 s also capable of complex formation with the tumor suppressor protein p53.
13 n regulating numerous proteins including the tumor suppressor protein p53.
14 of E2F97 resulted in down-regulation of the tumor suppressor protein p53.
15 n this report show that BKV TAg can bind the tumor suppressor protein p53.
16 dalton protein that inactivates the cellular tumor suppressor protein p53.
17 m that is dependent on the activation of the tumor suppressor protein p53.
18 factors such as PPARgamma, NFkappaB, and the tumor suppressor protein p53.
19 aration of reduced and oxidized forms of the tumor suppressor protein p53.
20 mor-associated HPV induce the degradation of tumor suppressor protein p53.
21 on of the tetramerization domain (TD) of the tumor suppressor protein p53.
22 gulating non-histone proteins, including the tumor suppressor protein p53.
23 ransferase enzyme SET8/PR-Set7 regulates the tumor suppressor protein p53.
24 derably the transcriptional network of human tumor suppressor protein p53.
25 ects, nucleophosmin is known to regulate the tumor suppressor protein p53.
26 into the intrinsically disordered tetrameric tumor suppressor protein p53.
27 tion is essential for the proper function of tumor suppressor protein p53.
28 could be partially rescued by removal of the tumor suppressor protein p53.
29 protein promotes apoptosis downstream of the tumor-suppressor protein p53.
30 ealed common signatures of activation of the tumor-suppressor protein p53.
31 ine mutations in TP53, the gene encoding the tumor-suppressor protein p53.
32 directly phosphorylating and activating the tumor-suppressor protein p53.
33 nit of S100B and target proteins such as the tumor suppressor protein, p53.
34 N1 gene product, interacts directly with the tumor suppressor protein, p53.
35 epresses the transcriptional activity of the tumor suppressor protein, p53.
36 of HCC through its ability to bind the human tumor suppressor protein, p53.
37 plasms were analysed for the presence of the tumor suppressor protein, p53.
38 to cancer progression by down-regulating the tumor suppressor protein, p53.
39 in has been shown to form a complex with the tumor suppressor protein p53, a known inducer of apoptos
40 ing is crucial to the protective role of the tumor suppressor protein p53, a nuclear phosphoprotein a
41 y regulate the activity and stability of the tumor suppressor protein p53--a cellular process initiat
46 ection, E1B-55K binds to and inactivates the tumor suppressor protein p53, allowing efficient replica
47 phosphorylation and increased levels of the tumor suppressor protein p53 and a cell cycle inhibitor
48 y regulate the activity and stability of the tumor suppressor protein p53 and are important molecular
49 hich correlate with the up-regulation of the tumor suppressor protein p53 and concurrent up-regulatio
50 es cell survival by decreasing levels of the tumor suppressor protein p53 and downstream target genes
52 Inhibition of the interaction between the tumor suppressor protein p53 and its negative regulators
53 ules selectively delivered recombinant human tumor suppressor protein p53 and its tumor-selective sup
54 molecular targets with the activators of the tumor suppressor protein p53 and NF-kappaB-p65, suggesti
55 zo(a)pyrene failed to significantly increase tumor suppressor protein p53 and p53-regulated growth-re
56 showed that EBNA3C can directly bind to the tumor suppressor protein p53 and repress its functions,
58 by nicotine results in the induction of the tumor suppressor protein p53 and the cdk inhibitor p21.
60 experimental approach was validated with the tumor suppressor protein p53 and the forkhead protein Fo
61 ell apoptosis in a pathway that involves the tumor suppressor protein p53 and the mitochondrial trans
62 not only suppresses apoptosis induced by the tumor suppressor protein p53 and the Myc oncoprotein but
63 sly unreported nuclear complexes between the tumor suppressor protein p53 and the pro-apoptotic prote
64 ing that there may be cross talk between the tumor suppressor protein p53 and WISP-1 signaling pathwa
65 eins involved in recombination and also with tumor suppressor proteins p53 and breast cancer suscepti
66 wth, was remarkably downregulated, while the tumor suppressor proteins p53 and p21 were substantially
68 on in the levels of pyridine nucleotides and tumor suppressor proteins p53 and p73, and a decrease in
69 SV40 large T antigen (T) inactivates the tumor suppressor proteins p53 and pRb, and can induce ce
72 ducts can associated with and inactivate the tumor suppressor proteins p53 and Rb (the retinoblastoma
73 ts interacting partners such as the cellular tumor suppressor proteins p53 and Rb, both in vitro and
77 is due in large part to perturbation of the tumor suppressor proteins p53 and the retinoblastoma (pR
79 ell cycle regulatory proteins, including the tumor suppressor proteins, p53 and p105Rb, in order to i
80 ontrol of infected cells by inactivating the tumor suppressor proteins, p53 and Rb, respectively.
83 tumor antigen (T-ag), which inactivates the tumor-suppressor proteins p53 and pRb family members.
84 periments showed that ORF-1 protein bound to tumor suppressor protein p53, and the ORF-1 binding doma
85 et for transcriptional downregulation by the tumor suppressor protein p53, and this repression can be
87 0B(beta beta) was found to interact with the tumor suppressor protein, p53, and inhibit its PKC-depen
88 1 cell cycle arrest through induction of the tumor suppressor protein, p53, and the cyclin-dependent
89 xpression of Zta results in induction of the tumor suppressor protein, p53, and the cyclin-dependent
90 apoptosis and autophagy; not reliant on the tumor suppressor protein p53; and effective against mous
95 n Chk1, increased phosphorylation of the p53 tumor suppressor protein (p53) at serine 18, and increas
96 dc14A and hCdc14B proteins interact with the tumor suppressor protein p53 both in vitro and in vivo.
97 ates the binding of mtrII oncoprotein to the tumor suppressor protein p53 both in vivo using transien
98 n not only suppress apoptosis induced by the tumor suppressor protein p53, but also permit efficient
99 ily in melanoma cells harboring a functional tumor suppressor protein p53, but much less efficiently
100 itiate cell death are thought to involve the tumor suppressor protein p53, but the degree to which th
101 verexpressed in many cancers, stabilizes the tumor suppressor protein p53 by abrogating its MDM2-depe
106 y regulate the activity and stability of the tumor suppressor protein p53, conferring tumor developme
107 Although the N-terminal BOX-I domain of the tumor suppressor protein p53 contains the primary dockin
113 reasing intrinsic disorder-cytochrome c, the tumor suppressor protein p53 DNA binding domain (p53 DBD
115 ferentiation defect that is dependent on the tumor suppressor protein p53 (encoded by Trp53 in mice)
116 but not the oncoprotein Myc, or loss of the tumor suppressor protein p53 (encoded by Trp53 in mice)
128 roliferation of breast cancer cells, whereas tumor suppressor protein p53 impedes proliferation of ce
129 , we found that uPA alters expression of the tumor suppressor protein p53 in Beas2B airway epithelial
130 ay format was used to detect unlabeled human tumor suppressor protein p53 in crude lysates, without a
133 the dynamics of the tetramers formed by the tumor suppressor protein p53 in single living cells.
134 s multiple lines of evidence implicating the tumor suppressor protein p53 in terminal differentiation
135 protein, Parc, and its role in anchoring the tumor suppressor protein p53 in the cytoplasm reveals ye
136 ly to be a transcription target of the human tumor-suppressor protein p53 in signaling apoptosis and
138 ells, binding of E1B-55kDa and E4orf6 to the tumor suppressor protein p53 inhibits its transcriptiona
140 te mechanism to ubiquitinate and degrade the tumor suppressor protein p53, involving interactions wit
150 Antagonizing MDM2 and MDMX to activate the tumor suppressor protein p53 is an attractive therapeuti
166 ial downstream effecter of this pathway, the tumor suppressor protein p53, is tightly regulated by co
173 gh transcriptionally dependent inhibition of tumor suppressor protein p53, normalization of the pro-a
174 lium leads to marked hyperacetylation of the tumor suppressor protein p53 on lysine 370, 379 and 383;
176 ition of c-Myc could be altered by depleting tumor suppressor protein p53 or its transcriptional targ
180 e acidic transactivation domain of the human tumor suppressor protein p53 (p53TAD) and the 70 kDa sub
182 t that two novel synthetic inhibitors of the tumor suppressor protein p53, pifithrin-alpha (PFT-alpha
195 g the degree to which it cooperates with the tumor suppressor protein p53, remain poorly understood.
196 ition of certain types of DNA lesions by the tumor suppressor protein, p53, represents one of the sev
198 lls are exposed to stressful conditions, the tumor suppressor protein p53 restrains growth by promoti
199 Mutations within conserved regions of the tumor suppressor protein, p53, result in oncogenic forms
200 knockdown of NS increase the activity of the tumor suppressor protein p53, resulting in cell cycle ar
201 ction (p.i.), followed by phosphorylation of tumor suppressor protein p53 Ser 15 at 3 to 6 h p.i., st
202 shown previously that NPCs deficient in the tumor suppressor protein p53 show significantly less dea
203 ponse to a variety of stimuli, including the tumor suppressor protein p53, that can mediate cell cycl
205 ressing temperature-sensitive mutants of the tumor suppressor protein p53, the viral oncogene protein
206 the mutant form seems to form a complex with tumor suppressor protein p53, thereby enhancing its intr
207 pansion of stromal fibroblasts that lack the tumor-suppressor protein p53 through a paracrine mechani
208 nges in small and large regions of the human tumor suppressor protein p53 to identify single amino-ac
209 cogenic human polyomavirus BK (BKV) with the tumor-suppressor protein p53 to understand the biology o
212 R-132 on proliferating cell nuclear antigen, tumor suppressor protein p53, transcription factor NF-ka
213 o induce the accumulation and acetylation of tumor suppressor protein p53 upon the cell cycle entry o
214 nk between mitochondrial dysfunction and the tumor suppressor protein p53 using a set of respiration-
216 dition, down-regulation of the pro-apoptotic tumor suppressor protein, p53, via PKB-mediated phosphor
217 eous shrinking: the intrinsically disordered tumor suppressor protein p53 was analyzed by using a com
220 M2 is an important negative regulator of the tumor suppressor protein p53 which regulates the express
221 and MDM4 are key negative regulators of the tumor suppressor protein p53, which are frequently upreg
223 rfamily trigger apoptosis independent of the tumor suppressor protein p53, which primarily affects DN
224 fection by human cytomegalovirus (HCMV), the tumor suppressor protein p53, which promotes efficient v
225 30-fold increase in the nuclear level of the tumor suppressor proteins p53 (wild type), pRb, and p130
226 zmB also induces a rapid accumulation of the tumor-suppressor protein p53 within target cells, which
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