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1 ed additionally for the tumor suppressor p53 protein (p53).
2 rization domain (TD) of the tumor suppressor protein p53.
3 ovarian tumor cell lines not expressing the protein p53.
4 one proteins, including the tumor suppressor protein p53.
5 SET8/PR-Set7 regulates the tumor suppressor protein p53.
6 criptional network of human tumor suppressor protein p53.
7 rylating and activating the tumor-suppressor protein p53.
8 in is known to regulate the tumor suppressor protein p53.
9 causes a rapid stabilization of the cellular protein p53.
10 for the proper function of tumor suppressor protein p53.
11 y rescued by removal of the tumor suppressor protein p53.
12 apoptosis downstream of the tumor-suppressor protein p53.
13 scriptional activity of the tumor suppressor protein p53.
14 cally disordered tetrameric tumor suppressor protein p53.
15 hibitory cytokines and the tumour-suppressor protein p53.
16 hibitor of signaling by the tumor suppressor protein p53.
17 proline-rich domain of the tumor suppressor protein p53.
18 a checkpoint involving the tumor suppressor protein p53.
19 es and hence stabilizes the tumor suppressor protein p53.
20 crease in the expression of the proapoptotic protein p53.
21 the proapoptotic BAX is the tumor suppressor protein p53.
22 ctivity is repressed by the tumor suppressor protein p53.
23 apid elevations of the DNA damage-responsive protein p53.
24 in a complex stabilized by tumor suppressor protein p53.
25 atures of activation of the tumor-suppressor protein p53.
26 int independently of the 'tumour suppressor' protein p53.
27 iptionally regulated by the tumor suppressor protein p53.
28 egradation of the cellular tumour-suppressor protein p53.
29 l negative regulator of the tumor suppressor protein p53.
30 teraction with the cellular tumor suppressor protein p53.
31 rous proteins including the tumor suppressor protein p53.
32 PARgamma, NFkappaB, and the tumor suppressor protein p53.
33 TP53, the gene encoding the tumor-suppressor protein p53.
34 d and oxidized forms of the tumor suppressor protein p53.
35 V induce the degradation of tumor suppressor protein p53.
36 utations in KRAS, BRAF, or PIK3CA, and tumor protein p53.
37 to assess mutations in the tumour-suppressor protein, p53.
38 target proteins such as the tumor suppressor protein, p53.
39 scription factors including the proapoptotic protein, p53.
40 interacts directly with the tumor suppressor protein, p53.
41 scriptional activity of the tumor suppressor protein, p53.
42 s ability to bind the human tumor suppressor protein, p53.
43 sed for the presence of the tumor suppressor protein, p53.
44 sion by down-regulating the tumor suppressor protein, p53.
47 to form a complex with the tumor suppressor protein p53, a known inducer of apoptosis, thereby stabi
48 the protective role of the tumor suppressor protein p53, a nuclear phosphoprotein and transcription
49 tivity and stability of the tumor suppressor protein p53--a cellular process initiated by MDM2 and/or
50 nce of Myc, AMPK-stabilized tumor suppressor protein p53 accumulates in the mitochondria and interact
53 inds to and inactivates the tumor suppressor protein p53, allowing efficient replication of the virus
55 and increased levels of the tumor suppressor protein p53 and a cell cycle inhibitor protein p21 (Waf1
56 tivity and stability of the tumor suppressor protein p53 and are important molecular targets for anti
57 th the up-regulation of the tumor suppressor protein p53 and concurrent up-regulation of the cyclin-d
58 affects the binding of the tumour suppressor protein p53 and correlates with decreased expression of
60 e in the expression of tumor suppressor gene protein p53 and elevation of the level of cyclin-depende
61 an form complexes with the tumour-suppressor protein p53 and generate high levels of reactive oxygen
63 the interaction between the tumor suppressor protein p53 and its negative regulators MDM2 and MDMX is
64 delivered recombinant human tumor suppressor protein p53 and its tumor-selective supervariant into ta
65 geal adenocarcinomas have mutations in tumor protein p53 and mutations that activate receptor-associa
67 with the activators of the tumor suppressor protein p53 and NF-kappaB-p65, suggesting similar mechan
68 d to significantly increase tumor suppressor protein p53 and p53-regulated growth-related protein p21
69 3C can directly bind to the tumor suppressor protein p53 and repress its functions, in part by blocki
70 at LANA interacts with the tumour suppressor protein p53 and represses its transcriptional activity.
74 oach was validated with the tumor suppressor protein p53 and the forkhead protein FoxI1 using genomic
75 a pathway that involves the tumor suppressor protein p53 and the mitochondrial translocation of p53.
76 ontaining target sequences in the checkpoint protein p53 and the nonsense-mediated mRNA decay (NMD) p
77 clear complexes between the tumor suppressor protein p53 and the pro-apoptotic protein Bax, in human
79 that physical interactions of other cellular proteins (p53 and par-4) with WT1 can modulate the funct
82 As were ubiquitin, the cell cycle-regulating proteins p53 and mdm-2, HSP70, the global transcriptiona
83 ning, expression of the senescent associated proteins p53 and p16INK4a, and apoptosis of CPCs, impair
84 ly downregulated, while the tumor suppressor proteins p53 and p21 were substantially upregulated foll
92 reover, the expressions of tumour suppressor proteins p53 and PTEN were upregulated along with the do
96 part to perturbation of the tumor suppressor proteins p53 and the retinoblastoma (pRB) family members
99 of somatic mutations in TP53 (encoding tumor protein p53) and PTEN (encoding phosphate and tensin hom
100 in the cell activates the tumour-suppressor protein p53, and failure of this activation leads to gen
101 ng enhanced degradation of tumour suppressor protein p53, and inhibition of gankyrin activity has the
102 ional downregulation by the tumor suppressor protein p53, and this repression can be shown to contrib
103 ensus binding site for the tumour suppressor protein p53, and we show by gel-retardation analysis tha
106 found to interact with the tumor suppressor protein, p53, and inhibit its PKC-dependent phosphorylat
107 ell cycle, the retinoblastoma-susceptibility protein, p53, and possibly DDX5 and DDX3 lead to enhance
108 tophagy; not reliant on the tumor suppressor protein p53; and effective against mouse models for B-ce
109 nstrate that IRF-1 and the tumour suppressor protein p53 are coordinately up-regulated during the res
112 trigger the induction of the stress response protein p53 are poorly understood but may involve altera
114 We also identified the tumor suppressor protein p53 as a mediator of podocyte apoptosis in cells
115 rogation of function of the tumor-suppressor protein p53 as a result of mutation of its gene, TP53, i
116 phosphorylation of the p53 tumor suppressor protein (p53) at serine 18, and increased p53 protein le
120 e we examine the genome-wide impact of tumor protein P53-binding protein 1 (53BP1) deficiency in lymp
123 ells harboring a functional tumor suppressor protein p53, but much less efficiently in p53-null mutan
124 are thought to involve the tumor suppressor protein p53, but the degree to which this factor contrib
125 any cancers, stabilizes the tumor suppressor protein p53 by abrogating its MDM2-dependent proteasomal
128 Here we report that the tumor suppressor protein p53 can associate with PXR and downregulate its
130 rotein, a homologue of the tumour-suppressor protein p53, can activate p53-responsive promoters and i
132 tivity and stability of the tumor suppressor protein p53, conferring tumor development and survival.
133 erminal BOX-I domain of the tumor suppressor protein p53 contains the primary docking site for MDM2,
135 ly, we show that Na and the tumor suppressor protein p53 cooperate to induce lytic gene expression in
138 mutations occurring in the tumour suppressor protein p53, demonstrating the applicability of the prop
140 disorder-cytochrome c, the tumor suppressor protein p53 DNA binding domain (p53 DBD), and the N-term
142 of Ku80 along with the cell cycle checkpoint protein, p53, dramatically increases the incidence of pr
143 on the conjugation of SUMO-1 with the target proteins p53, E1B, and promyelocytic leukemia protein an
144 ct that is dependent on the tumor suppressor protein p53 (encoded by Trp53 in mice) and is characteri
145 protein Myc, or loss of the tumor suppressor protein p53 (encoded by Trp53 in mice) further accelerat
146 eceptor alpha (ERalpha) and tumor suppressor protein p53 exert opposing effects on cellular prolifera
148 Under normal conditions, tumor suppressor protein p53 exists in the cell in its latent form and is
149 evious assumptions that the tumor suppressor protein p53 exists primarily and functionally as a singl
150 ibe the oxidation of a cell-cycle regulatory protein, p53, from a distance through DNA-mediated CT.
153 -alpha, an inhibitor of the tumor suppressor protein p53, had no effect on ROS generation but did blo
154 mothripsis, and a simpler genotype, WT tumor protein p53, had relatively few SNVs (average of 5.9 per
159 2 (HDM2), which binds to and inactivates the protein p53, has been linked to tumor aggressiveness and
160 he roles and actions of the tumor suppressor protein p53 have been extensively studied with regard to
162 pidermal patches that stain positive for p53 protein (p53 immunopositive patches, PIPs), which are co
163 reast cancer cells, whereas tumor suppressor protein p53 impedes proliferation of cells with genomic
164 PA alters expression of the tumor suppressor protein p53 in Beas2B airway epithelial cells in both a
165 d to detect unlabeled human tumor suppressor protein p53 in crude lysates, without any purification s
166 Lysine acetylation of the tumor suppressor protein p53 in response to a wide variety of cellular st
168 ription target of the human tumor-suppressor protein p53 in signaling apoptosis and growth suppressio
170 of evidence implicating the tumor suppressor protein p53 in terminal differentiation of the renal epi
171 d its role in anchoring the tumor suppressor protein p53 in the cytoplasm reveals yet another level o
174 It depends on the growth regulator p53 and a protein p53 induces, the cyclin dependent kinase inhibit
175 er and CCCH-type domain 1 (RC3H1), and tumor protein p53-inducible protein 11 (TP53I11) interacted wi
176 E1B-55kDa and E4orf6 to the tumor suppressor protein p53 inhibits its transcriptional activity and ca
178 biquitinate and degrade the tumor suppressor protein p53, involving interactions with the N-terminal
179 Improper function of the tumor suppressor protein p53 is a contributing factor in many human cance
188 M2 and MDMX to activate the tumor suppressor protein p53 is an attractive therapeutic paradigm for th
192 s study, we report that the tumor suppressor protein p53 is essential for the induction of cell death
193 he transcription factor and tumor suppressor protein p53 is frequently inactivated in human cancers.
196 al cellular conditions, the tumor suppressor protein p53 is kept at low levels in part due to ubiquit
201 In unstressed cells, the tumor suppressor protein p53 is present in a latent state and is maintain
205 he C-terminal domain of the tumor suppressor protein p53 is the site of non-specific DNA binding.
210 er the tumor suppressor TP53 (coding for the protein p53) is hypermutable at some stage of carcinogen
211 The TP53 gene, encoding tumour suppressor protein p53, is located on the short arm of chromosome 1
212 fecter of this pathway, the tumor suppressor protein p53, is tightly regulated by controlled degradat
213 provides evidence that the tumor suppressor protein, p53, is a transcriptional repressor of PKD1.
220 rate the potential biological role of the TS protein-p53 mRNA interaction, Western immunoblot analysi
223 ns in cultured cancer cells with TP53 (tumor protein p53) mutations, in cells from patients with nons
224 lly dependent inhibition of tumor suppressor protein p53, normalization of the pro-apoptotic Bax/Bcl-
225 ked hyperacetylation of the tumor suppressor protein p53 on lysine 370, 379 and 383; these post-trans
226 , ATR phosphorylates the genome surveillance protein p53 on serine 15, a site which is up-regulated i
228 uld be altered by depleting tumor suppressor protein p53 or its transcriptional target p21(CIP/WAF).
229 lls deficient in either the tumor suppressor proteins p53 or Bax, apoptosis was least affected in the
230 Moreover, knocking down tumor suppressor proteins p53 or pRB using small interfering RNA signific
232 of key cell cycle regulators (retinoblastoma protein, p53, p21(waf1/Cip1), and p16(INK4A)), and senes
233 onally dead variant of the tumour-suppressor protein p53 (p53(25,26,53,54)), along with a wild-type a
234 that none of the 27 patients with both tumor protein p53 (p53) and v-Ki-ras2 Kirsten rat sarcoma vira
235 ivation domain of the human tumor suppressor protein p53 (p53TAD) and the 70 kDa subunit of human rep
236 tain coat protein I (COPI) and the recycling protein p53/p58, suggesting that the vesicles traffic in
238 synthetic inhibitors of the tumor suppressor protein p53, pifithrin-alpha (PFT-alpha) and Z-1-117, ar
251 udies revealed two unique functions for this protein: p53 regulates cellular energy metabolism and an
253 types of DNA lesions by the tumor suppressor protein, p53, represents one of the several downstream f
256 o stressful conditions, the tumor suppressor protein p53 restrains growth by promoting an arrested ce
258 lowed by phosphorylation of tumor suppressor protein p53 Ser 15 at 3 to 6 h p.i., stabilizing p53 lev
259 that NPCs deficient in the tumor suppressor protein p53 show significantly less death after exposure
260 y of stimuli, including the tumor suppressor protein p53, that can mediate cell cycle arrest through
262 eems to form a complex with tumor suppressor protein p53, thereby enhancing its intracellular level t
263 forming a complex with the tumour-suppressor protein p53, thereby stabilizing it and enhancing its fu
265 large regions of the human tumor suppressor protein p53 to identify single amino-acid substitutions
268 the effects for SNP309 and the related tumor protein p53 (TP53) Arg72Pro are inconsistent among publi
269 ma viral oncogene homolog B (BRAF) and tumor protein p53 (TP53) mutations cooccur in a high proportio
270 arcomatoid elements acquired biallelic tumor protein p53 (TP53) mutations in 32% of tumors (P = 5.47
271 cancers, TDP tumors conjointly exhibit tumor protein p53 (TP53) mutations, disruption of breast cance
272 d at 17p13, only 500-kb centromeric of tumor protein p53 (Tp53), and is codeleted with Tp53, we propo
273 emonstrates the involvement of BCL6 in tumor protein p53 (TP53), erythroblastic leukemia viral oncoge
276 primary mouse epithelial cells lacking tumor protein p53 (TP53, best known as p53) in the presence of
277 ating cell nuclear antigen, tumor suppressor protein p53, transcription factor NF-kappaB p50 and its
278 with somatic loss of transformation-related protein p53 (Trp53) function and/or overexpression of hu
279 at, together with a variety of other nuclear proteins, p53 undergoes extensive poly(ADP-ribosyl)ation
280 ed expression of Bcl-2 homology 3 (BH3)-only protein p53 up-regulated modulator of apoptosis (PUMA),
281 vels of p53 and the p53-related proapoptotic proteins p53-up-regulated modulator of apoptosis (PUMA)
282 mulation and acetylation of tumor suppressor protein p53 upon the cell cycle entry of hair follicle e
284 ently showed a critical role of the BH3-only protein p53 upregulated modulator of apoptosis (PUMA) in
287 ondrial dysfunction and the tumor suppressor protein p53 using a set of respiration-deficient (Res(-)
289 type activation of temperature-sensitive p53 protein (p53 val) at permissive temperature in M1-t-p53
290 lation of the pro-apoptotic tumor suppressor protein, p53, via PKB-mediated phosphorylation of MDM2 m
291 he intrinsically disordered tumor suppressor protein p53 was analyzed by using a combination of ion m
293 ound that expression of the tumor suppressor protein p53 was higher in MCH(-/-) mice at 9 and 19 mont
294 t negative regulator of the tumor suppressor protein p53 which regulates the expression of many genes
295 negative regulators of the tumor suppressor protein p53, which are frequently upregulated in cancer
296 gest a novel mechanism by which the cellular protein p53, which is involved in both transcriptional r
297 poptosis independent of the tumor suppressor protein p53, which primarily affects DNA damage-induced
298 cytomegalovirus (HCMV), the tumor suppressor protein p53, which promotes efficient viral gene express
299 in the nuclear level of the tumor suppressor proteins p53 (wild type), pRb, and p130/Rb2 and of the p
300 a rapid accumulation of the tumor-suppressor protein p53 within target cells, which seems to be invol
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