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1 fork recovery is mediated through the PALB2 tumor suppressor protein.
2 Tazarotene-induced gene 3 (TIG3) is a tumor suppressor protein.
3 of the human homologue of Mod5, TRIT1, as a tumor suppressor protein.
4 h SIRT2 may function, at least in part, as a tumor suppressor protein.
5 nt loss of function of the von Hippel-Lindau tumor suppressor protein.
6 and in cancer via interaction with the DAL-1 tumor suppressor protein.
7 gene doc-1 (deleted in oral cancer 1), is a tumor suppressor protein.
8 ubsequently stabilizes and activates the p53 tumor suppressor protein.
9 The transcription factor p53 is a key tumor suppressor protein.
10 of mutations in the von Hippel Lindau (VHL) tumor suppressor protein.
11 ied, including the c-JUN oncoprotein and p53 tumor suppressor protein.
12 ability of E7 to inhibit the retinoblastoma tumor suppressor protein.
13 the functionally critical UCH domain in this tumor suppressor protein.
14 istone acetyltransferase (HAT) complex and a tumor suppressor protein.
15 en shown to be identical to Nit2, a putative tumor suppressor protein.
16 ple, the transcriptional activity of the p53 tumor suppressor protein.
17 ed, suggesting that HBP1 may be an important tumor suppressor protein.
18 These data reveal the role of A20 as a tumor suppressor protein.
19 errant mitosis by directly regulating the Rb tumor suppressor protein.
20 by the expression of a chosen oncoprotein or tumor suppressor protein.
21 a significant role in the regulation of the tumor suppressor protein.
22 in the phosphatase and tensin homolog (PTEN) tumor suppressor protein.
23 s, and binding of inhibitors such as the p27 tumor suppressor protein.
24 lysis to demonstrate the role of MOAP-1 as a tumor suppressor protein.
25 development of small molecule activators of tumor suppressor proteins.
26 the cytoplasmic mislocalization of multiple tumor suppressor proteins.
27 ol systems in the degradative fate of mutant tumor suppressor proteins.
28 roteins inactivated the function of cellular tumor suppressor proteins.
29 program controlled by the p53 and p16(INK4a) tumor suppressor proteins.
30 gulate the expression of PTEN and p53-family tumor-suppressor proteins.
43 are expected for oncoproteins, we found that tumor suppressor proteins also exhibit strong biases tow
44 ased HIF-1alpha binding to von Hippel-Lindau tumor suppressor protein, an E3 ligase component and an
45 sis for understanding the role of menin as a tumor suppressor protein and as an oncogenic co-factor o
46 g TS and RR was enriched with retinoblastoma tumor suppressor protein and histone H3 tri-methylated a
47 cer include suppressing induction of the p53 tumor suppressor protein and maintaining metabolic funct
48 and tensin homolog deleted on chromosome 10) tumor suppressor protein and phosphate-depended kinase 1
49 sequence-specific DNA-binding domain of the tumor suppressor protein and preventing it from transcri
50 resents evidence that de-ph-S302-CUGBP1 is a tumor suppressor protein and that the Gank-UPS-mediated
52 n homolog of the Drosophila polycomb L(3)MBT tumor suppressor protein and thus a candidate tumor supp
53 s the key mediator of nuclear export of many tumor suppressor proteins and is overexpressed in human
54 ) function, leads to nuclear accumulation of tumor suppressor proteins, and induces cancer cell death
55 gulated by the retinoblastoma (RB) family of tumor suppressor proteins, and virus-encoded oncogenes d
56 diploid RPE-1 cells, either by depleting the tumor suppressor protein APC or the kinesin-13 protein M
57 asmic dynein, the adenomatous polyposis coli tumor suppressor protein (APC), and glycogen synthase ki
58 ctasia mutated (ATM) kinase and H2AX histone tumor suppressor proteins are each critical for maintena
63 ell, Chen et al. (2017) demonstrate that the tumor suppressor protein ARF sensitizes cancer cells to
64 study, we have examined the roles of the p53 tumor suppressor protein, as well as its downstream targ
67 s recognized multiple putative oncogenic and tumor suppressor protein binding sites in the AKR1B10 pr
68 show that DIM up-regulates expression of the tumor suppressor protein BRCA1 in carcinoma and normal c
71 air-mediated helicase unloading involves the tumor suppressor protein BRCA1, which acts upstream of M
73 otif is reminiscent of the FVPP motif in the tumor suppressor protein BRCA2 that mediates DMC1 intera
74 s as a crucial negative regulator of the p53 tumor suppressor protein by antagonizing p53 transactiva
75 rmore, we find that TRIB2 relieves the liver tumor suppressor protein C/EBPalpha-mediated inhibition
77 oto-oncogenes can up-regulate Pol I, whereas tumor suppressor proteins can inhibit rRNA synthesis.
78 rticles containing the gene encoding the p53 tumor suppressor protein (chi-p53) and/or doxorubicin (D
79 rous transcription factors including the p53 tumor suppressor protein constitutes a vital early step
81 g extracts and human cells, we show that the tumor suppressor protein CtIP plays a critical role in t
83 s revealed increased nuclear accumulation of tumor suppressor proteins, decreased cell proliferation,
85 ads to microRNA-21 (miR-21) production and a tumor suppressor protein (e.g. PDCD4 (program cell death
86 y TGFbeta is dependent on the retinoblastoma tumor suppressor protein/E2 promoter binding factor (pRb
87 ike protein, also known as schwannomin) is a tumor suppressor protein encoded by the neurofibromatosi
89 Members of the Myb oncoprotein and E2F-Rb tumor suppressor protein families are present within the
90 Fanconi anemia (FA) DNA repair pathway, the tumor suppressor proteins FANCI and FANCD2 (the ID compl
91 Argast et al. has shown that plexin B1 is a tumor-suppressor protein for melanoma metastasis in a mo
92 1, the Semaphorin 4D (Sema4D) receptor, is a tumor-suppressor protein for melanoma, which functions,
94 analysis also demonstrated that recovery of tumor suppressor protein function is possible, indicatin
98 This process results in the reduction of a tumor suppressor protein (HOXD10), RhoA/RhoC up-regulati
99 roduction, leading to the down-regulation of tumor suppressor protein (HOXD10), RhoGTPase-ROK activat
101 r, which regulates the transcription of this tumor suppressor protein in a TSC2-dependent manner.
102 ssion, and decreased nuclear levels of BRCA1 tumor suppressor protein in invasive breast carcinomas.
103 earliest detectable epigenetically silenced tumor suppressor proteins in cancer, and we speculate th
104 xin B1 is predicted to function as a classic tumor-suppressor protein in melanoma, in part through su
106 it CRM-1 and promote nuclear accumulation of tumor-suppressor proteins in pancreatic cancer cells.
107 clude ARF and P16INK4A, both of which encode tumor suppressor proteins, in both human and mouse retin
108 ncogenic transformation by inhibition of key tumor suppressor proteins, including p53 and members of
109 oncogenic proteins, decreased expression of tumor suppressor protein, increased proliferation, decre
113 nterferon-regulated transcription factor and tumor suppressor protein IRF-1 is predicted to be largel
117 lar senescence through activation of the p53 tumor suppressor protein is a new option for treating pr
119 special note is the observation that the p53 tumor suppressor protein is confined to the open chromat
124 ow that Beclin 1, an essential autophagy and tumor suppressor protein, is a target of the protein kin
126 ic response element, in conjunction with the tumor suppressor protein Kruppel-like factor 6 functioni
128 r cells, and this is associated with reduced tumor suppressor protein level and enhanced cell surviva
130 tal Cell, Jossin et al. (2017) show that the tumor suppressor protein Lgl1 interacts with N-cadherin
131 ical differences in mTORC1 regulation by the tumor suppressor proteins Lkb1 and Tsc1/Tsc2 may underli
141 ascade have been shown to function either as tumor suppressor proteins or as oncogenes in multiple hu
144 arcinomas (CxCaRNA(+)), and the HPV-targeted tumor suppressor protein p16(INK4a) as markers for HPV i
145 sive breast cancer cells, down-regulates the tumor suppressor proteins p16(INK4A), p21(WAF1), and p53
147 of cells incubated with KPT-185 accumulated tumor-suppressor proteins (p27, FOXO, p73, and prostate
148 ferentiation defect that is dependent on the tumor suppressor protein p53 (encoded by Trp53 in mice)
149 but not the oncoprotein Myc, or loss of the tumor suppressor protein p53 (encoded by Trp53 in mice)
150 Under influence of Myc, AMPK-stabilized tumor suppressor protein p53 accumulates in the mitochon
152 phosphorylation and increased levels of the tumor suppressor protein p53 and a cell cycle inhibitor
153 es cell survival by decreasing levels of the tumor suppressor protein p53 and downstream target genes
154 Inhibition of the interaction between the tumor suppressor protein p53 and its negative regulators
155 ules selectively delivered recombinant human tumor suppressor protein p53 and its tumor-selective sup
156 showed that EBNA3C can directly bind to the tumor suppressor protein p53 and repress its functions,
158 verexpressed in many cancers, stabilizes the tumor suppressor protein p53 by abrogating its MDM2-depe
164 reasing intrinsic disorder-cytochrome c, the tumor suppressor protein p53 DNA binding domain (p53 DBD
168 ay format was used to detect unlabeled human tumor suppressor protein p53 in crude lysates, without a
169 the dynamics of the tetramers formed by the tumor suppressor protein p53 in single living cells.
172 Antagonizing MDM2 and MDMX to activate the tumor suppressor protein p53 is an attractive therapeuti
174 lium leads to marked hyperacetylation of the tumor suppressor protein p53 on lysine 370, 379 and 383;
179 ction (p.i.), followed by phosphorylation of tumor suppressor protein p53 Ser 15 at 3 to 6 h p.i., st
180 nges in small and large regions of the human tumor suppressor protein p53 to identify single amino-ac
181 o induce the accumulation and acetylation of tumor suppressor protein p53 upon the cell cycle entry o
182 nk between mitochondrial dysfunction and the tumor suppressor protein p53 using a set of respiration-
183 eous shrinking: the intrinsically disordered tumor suppressor protein p53 was analyzed by using a com
184 y regulate the activity and stability of the tumor suppressor protein p53, conferring tumor developme
185 te mechanism to ubiquitinate and degrade the tumor suppressor protein p53, involving interactions wit
187 knockdown of NS increase the activity of the tumor suppressor protein p53, resulting in cell cycle ar
189 and MDM4 are key negative regulators of the tumor suppressor protein p53, which are frequently upreg
190 fection by human cytomegalovirus (HCMV), the tumor suppressor protein p53, which promotes efficient v
191 y regulate the activity and stability of the tumor suppressor protein p53--a cellular process initiat
201 apoptosis and autophagy; not reliant on the tumor suppressor protein p53; and effective against mous
202 wth, was remarkably downregulated, while the tumor suppressor proteins p53 and p21 were substantially
203 ts interacting partners such as the cellular tumor suppressor proteins p53 and Rb, both in vitro and
206 zmB also induces a rapid accumulation of the tumor-suppressor protein p53 within target cells, which
209 n Chk1, increased phosphorylation of the p53 tumor suppressor protein (p53) at serine 18, and increas
213 In summary, our phosphorylation analysis of tumor suppressor protein PALB2 uncovers new layers of re
214 e for the cyclin D1/Cdk4/pRb (retinoblastoma tumor suppressor protein) pathway in delayed neuronal de
216 This process results in a decrease of a tumor suppressor protein (PDCD4), and an upregulation of
217 (human homolog of the Drosophila discs large tumor suppressor protein) PDZ (postsynaptic density/disc
220 ukemic HSCs in BM requires inhibition of the tumor suppressor protein phosphatase 2A (PP2A) and expre
221 we have demonstrated that activation of the tumor suppressor protein phosphatase 2A (PP2A), a negati
222 multiple cellular processes, inhibiting the tumor suppressor protein phosphatase 2A (PP2A), and inhi
224 trocytes deficient in the major glioblastoma tumor suppressor protein phosphatase and tensin homolog
232 nding the cellular life span by sequestering tumor suppressor proteins pRB and p53 in virus-transform
233 tion, UL97 phosphorylates the retinoblastoma tumor suppressor protein (pRb) on sites ordinarily phosp
235 key downstream target of the retinoblastoma tumor suppressor protein (pRB), which is frequently inac
236 that inactivate the cellular retinoblastoma tumor suppressor protein (pRb), which normally functions
237 nd hypophosphorylation of the retinoblastoma tumor suppressor protein (pRb), with no effect on cyclin
239 previously showed that inactivating the p53 tumor suppressor protein prevents neural tube and cardia
240 MO, which in turn promotes expression of the tumor suppressor protein promyelocytic leukemia (PML).
244 d predictive markers, such as alterations of tumor suppressor proteins PTEN or p53, to augment curren
246 sing pathway including the von Hippel-Lindau tumor suppressor protein (pVHL) and the hypoxia inducibl
247 endent and -independent functions of the VHL tumor suppressor protein (pVHL) can contribute to tumor
248 tered metabolism in cancer cells related to: tumor suppressor protein (pVHL) function, the histone ac
250 oded proteins with cell cycle regulators and tumor suppressor proteins, raising the possibility that
253 pment of liver cancer is a neutralization of tumor suppressor proteins Rb, p53, hepatocyte nuclear fa
256 virus (HCV) downregulates the retinoblastoma tumor suppressor protein (Rb), a central cell cycle regu
258 N-terminal domain of the retinoblastoma (Rb) tumor suppressor protein (RbN) harbors in-frame exon del
259 biopsies showed nuclear accumulation of key tumor-suppressor proteins, reduction of cell proliferati
263 was further ratified by the upregulation of tumor suppressor protein retinoblastoma, which repressed
265 C-terminal domain (RbC) is necessary for the tumor suppressor protein's activities in growth suppress
271 st cancer susceptibility gene 1 (BRCA1) is a tumor suppressor protein that functions to maintain geno
274 on-associated miRNA-mediated regulation of a tumor suppressor protein that has the ability to influen
277 bunit of an SCF ubiquitin ligase and a major tumor-suppressor protein that is altered in several huma
278 homolog deleted on chromosome 10 (PTEN) is a tumor-suppressor protein that regulates phosphatidylinos
279 though RASSF1A is now considered a bona fide tumor suppressor protein, the role of MOAP-1 as a tumor
280 proteins and host cell cycle regulators and tumor suppressor proteins, the relevance of these observ
281 Small molecule mediated stabilization of p53 tumor suppressor protein through sumoylation is a promis
282 method showed that translocation of the p53 tumor-suppressor protein to the perinucleus in immortali
283 By providing a means to restore a functional tumor-suppressor protein to tumor cells, PTEN-Long may h
285 ntranslated region (3'UTR) of the mRNA for a tumor suppressor protein, tumor protein 53-induced nucle
286 The Ras-assocation domain family (RASSF) of tumor suppressor proteins until recently contained six p
288 specific disruption of the von Hippel-Lindau tumor suppressor protein (VHL) resulted in constitutive
289 tion of genes encoding the von Hippel-Lindau tumor suppressor protein (Vhl), hypoxia-inducible factor
292 residues creates binding sites for the COP1 tumor suppressor protein, which is an ubiquitin ligase c
293 f cancers with defects in the BRCA1 or BRCA2 tumor suppressor proteins, which are involved in the rep
297 ated, pro-apoptotic peptide derived from p53 tumor suppressor protein with a human cancer cell line.
298 ortance of FAK following deletion of the Apc tumor suppressor protein within the intestinal epitheliu
299 9 locus harbors an imprinted gene encoding a tumor suppressor protein within the long-sought WT2 locu
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