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1 in the phosphatase and tensin homolog (PTEN) tumor suppressor protein.
2 lysis to demonstrate the role of MOAP-1 as a tumor suppressor protein.
3 (Cip1) cyclin-dependent kinase inhibitor and tumor suppressor protein.
4 fork recovery is mediated through the PALB2 tumor suppressor protein.
5 Tazarotene-induced gene 3 (TIG3) is a tumor suppressor protein.
6 of the human homologue of Mod5, TRIT1, as a tumor suppressor protein.
7 h SIRT2 may function, at least in part, as a tumor suppressor protein.
8 nt loss of function of the von Hippel-Lindau tumor suppressor protein.
9 and in cancer via interaction with the DAL-1 tumor suppressor protein.
10 gene doc-1 (deleted in oral cancer 1), is a tumor suppressor protein.
11 ubsequently stabilizes and activates the p53 tumor suppressor protein.
12 The transcription factor p53 is a key tumor suppressor protein.
13 of mutations in the von Hippel Lindau (VHL) tumor suppressor protein.
14 ied, including the c-JUN oncoprotein and p53 tumor suppressor protein.
15 ability of E7 to inhibit the retinoblastoma tumor suppressor protein.
16 a significant role in the regulation of the tumor suppressor protein.
17 s, and binding of inhibitors such as the p27 tumor suppressor protein.
18 the functionally critical UCH domain in this tumor suppressor protein.
19 roteins inactivated the function of cellular tumor suppressor proteins.
20 program controlled by the p53 and p16(INK4a) tumor suppressor proteins.
21 increase in biosynthesis of miR-21-regulated tumor suppressor proteins.
22 the cytoplasmic mislocalization of multiple tumor suppressor proteins.
23 ol systems in the degradative fate of mutant tumor suppressor proteins.
24 is by altering the activity of oncogenic and tumor suppressor proteins.
25 development of small molecule activators of tumor suppressor proteins.
26 bor a high prevalence of pDGVs that truncate tumor suppressor proteins.
38 sly shown that striatin colocalizes with the tumor suppressor protein adenomatous polyposis coli in t
40 are expected for oncoproteins, we found that tumor suppressor proteins also exhibit strong biases tow
41 ased HIF-1alpha binding to von Hippel-Lindau tumor suppressor protein, an E3 ligase component and an
42 sis for understanding the role of menin as a tumor suppressor protein and as an oncogenic co-factor o
43 g TS and RR was enriched with retinoblastoma tumor suppressor protein and histone H3 tri-methylated a
44 cer include suppressing induction of the p53 tumor suppressor protein and maintaining metabolic funct
45 sequence-specific DNA-binding domain of the tumor suppressor protein and preventing it from transcri
46 resents evidence that de-ph-S302-CUGBP1 is a tumor suppressor protein and that the Gank-UPS-mediated
48 n homolog of the Drosophila polycomb L(3)MBT tumor suppressor protein and thus a candidate tumor supp
49 s the key mediator of nuclear export of many tumor suppressor proteins and is overexpressed in human
50 A-encoded products form complexes with other tumor suppressor proteins and with the recombinase enzym
51 s responsible for the nuclear export of many tumor-suppressor proteins and viral ribonucleoproteins.
53 ) function, leads to nuclear accumulation of tumor suppressor proteins, and induces cancer cell death
54 gulated by the retinoblastoma (RB) family of tumor suppressor proteins, and virus-encoded oncogenes d
56 asmic dynein, the adenomatous polyposis coli tumor suppressor protein (APC), and glycogen synthase ki
57 ctasia mutated (ATM) kinase and H2AX histone tumor suppressor proteins are each critical for maintena
61 ell, Chen et al. (2017) demonstrate that the tumor suppressor protein ARF sensitizes cancer cells to
62 study, we have examined the roles of the p53 tumor suppressor protein, as well as its downstream targ
65 entify a new role for these well-established tumor suppressor proteins at an early stage of the cellu
68 air-mediated helicase unloading involves the tumor suppressor protein BRCA1, which acts upstream of M
71 otif is reminiscent of the FVPP motif in the tumor suppressor protein BRCA2 that mediates DMC1 intera
72 s as a crucial negative regulator of the p53 tumor suppressor protein by antagonizing p53 transactiva
73 rmore, we find that TRIB2 relieves the liver tumor suppressor protein C/EBPalpha-mediated inhibition
75 rticles containing the gene encoding the p53 tumor suppressor protein (chi-p53) and/or doxorubicin (D
76 rous transcription factors including the p53 tumor suppressor protein constitutes a vital early step
78 g extracts and human cells, we show that the tumor suppressor protein CtIP plays a critical role in t
80 s revealed increased nuclear accumulation of tumor suppressor proteins, decreased cell proliferation,
82 y TGFbeta is dependent on the retinoblastoma tumor suppressor protein/E2 promoter binding factor (pRb
83 ike protein, also known as schwannomin) is a tumor suppressor protein encoded by the neurofibromatosi
86 Members of the Myb oncoprotein and E2F-Rb tumor suppressor protein families are present within the
87 Fanconi anemia (FA) DNA repair pathway, the tumor suppressor proteins FANCI and FANCD2 (the ID compl
88 Argast et al. has shown that plexin B1 is a tumor-suppressor protein for melanoma metastasis in a mo
89 1, the Semaphorin 4D (Sema4D) receptor, is a tumor-suppressor protein for melanoma, which functions,
91 analysis also demonstrated that recovery of tumor suppressor protein function is possible, indicatin
94 This process results in the reduction of a tumor suppressor protein (HOXD10), RhoA/RhoC up-regulati
95 roduction, leading to the down-regulation of tumor suppressor protein (HOXD10), RhoGTPase-ROK activat
98 ssion, and decreased nuclear levels of BRCA1 tumor suppressor protein in invasive breast carcinomas.
99 earliest detectable epigenetically silenced tumor suppressor proteins in cancer, and we speculate th
100 xin B1 is predicted to function as a classic tumor-suppressor protein in melanoma, in part through su
102 it CRM-1 and promote nuclear accumulation of tumor-suppressor proteins in pancreatic cancer cells.
103 e propose that WASp functions as a putative "tumor-suppressor" protein in normal T and B cells, and "
104 clude ARF and P16INK4A, both of which encode tumor suppressor proteins, in both human and mouse retin
105 ncogenic transformation by inhibition of key tumor suppressor proteins, including p53 and members of
106 oncogenic proteins, decreased expression of tumor suppressor protein, increased proliferation, decre
108 orces nuclear accumulation and activation of tumor suppressor proteins, inhibits nuclear factor kappa
111 nterferon-regulated transcription factor and tumor suppressor protein IRF-1 is predicted to be largel
115 lar senescence through activation of the p53 tumor suppressor protein is a new option for treating pr
120 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
129 tal Cell, Jossin et al. (2017) show that the tumor suppressor protein Lgl1 interacts with N-cadherin
130 ical differences in mTORC1 regulation by the tumor suppressor proteins Lkb1 and Tsc1/Tsc2 may underli
142 arcinomas (CxCaRNA(+)), and the HPV-targeted tumor suppressor protein p16(INK4a) as markers for HPV i
143 sive breast cancer cells, down-regulates the tumor suppressor proteins p16(INK4A), p21(WAF1), and p53
145 of cells incubated with KPT-185 accumulated tumor-suppressor proteins (p27, FOXO, p73, and prostate
146 ferentiation defect that is dependent on the tumor suppressor protein p53 (encoded by Trp53 in mice)
147 but not the oncoprotein Myc, or loss of the tumor suppressor protein p53 (encoded by Trp53 in mice)
148 Under influence of Myc, AMPK-stabilized tumor suppressor protein p53 accumulates in the mitochon
150 phosphorylation and increased levels of the tumor suppressor protein p53 and a cell cycle inhibitor
151 es cell survival by decreasing levels of the tumor suppressor protein p53 and downstream target genes
152 Inhibition of the interaction between the tumor suppressor protein p53 and its negative regulators
153 ules selectively delivered recombinant human tumor suppressor protein p53 and its tumor-selective sup
154 showed that EBNA3C can directly bind to the tumor suppressor protein p53 and repress its functions,
156 verexpressed in many cancers, stabilizes the tumor suppressor protein p53 by abrogating its MDM2-depe
162 reasing intrinsic disorder-cytochrome c, the tumor suppressor protein p53 DNA binding domain (p53 DBD
166 ay format was used to detect unlabeled human tumor suppressor protein p53 in crude lysates, without a
167 the dynamics of the tetramers formed by the tumor suppressor protein p53 in single living cells.
170 Antagonizing MDM2 and MDMX to activate the tumor suppressor protein p53 is an attractive therapeuti
173 lium leads to marked hyperacetylation of the tumor suppressor protein p53 on lysine 370, 379 and 383;
174 3-3 with the recognition motif of either the tumor suppressor protein p53 or the oncogenic transcript
178 nges in small and large regions of the human tumor suppressor protein p53 to identify single amino-ac
179 o induce the accumulation and acetylation of tumor suppressor protein p53 upon the cell cycle entry o
180 nk between mitochondrial dysfunction and the tumor suppressor protein p53 using a set of respiration-
181 eous shrinking: the intrinsically disordered tumor suppressor protein p53 was analyzed by using a com
182 MDMX have been reported as activators of the tumor suppressor protein p53 with therapeutic potential.
183 y regulate the activity and stability of the tumor suppressor protein p53, conferring tumor developme
184 te mechanism to ubiquitinate and degrade the tumor suppressor protein p53, involving interactions wit
187 and MDM4 are key negative regulators of the tumor suppressor protein p53, which are frequently upreg
188 fection by human cytomegalovirus (HCMV), the tumor suppressor protein p53, which promotes efficient v
198 apoptosis and autophagy; not reliant on the tumor suppressor protein p53; and effective against mous
199 wth, was remarkably downregulated, while the tumor suppressor proteins p53 and p21 were substantially
200 ssential in this process by inactivating the tumor suppressor proteins p53 and Rb, respectively, in a
202 eltaIEC)) and mice that also had deletion of tumor-suppressor protein p53 (H2b/p53(DeltaIEC)); we com
205 zmB also induces a rapid accumulation of the tumor-suppressor protein p53 within target cells, which
206 lation of lysine residue(s) of histones, the tumor-suppressor protein p53, and splicing regulatory pr
209 n Chk1, increased phosphorylation of the p53 tumor suppressor protein (p53) at serine 18, and increas
214 In summary, our phosphorylation analysis of tumor suppressor protein PALB2 uncovers new layers of re
216 e for the cyclin D1/Cdk4/pRb (retinoblastoma tumor suppressor protein) pathway in delayed neuronal de
218 This process results in a decrease of a tumor suppressor protein (PDCD4), and an upregulation of
219 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 tion, UL97 phosphorylates the retinoblastoma tumor suppressor protein (pRb) on sites ordinarily phosp
234 key downstream target of the retinoblastoma tumor suppressor protein (pRB), which is frequently inac
235 previously showed that inactivating the p53 tumor suppressor protein prevents neural tube and cardia
236 MO, which in turn promotes expression of the tumor suppressor protein promyelocytic leukemia (PML).
239 d predictive markers, such as alterations of tumor suppressor proteins PTEN or p53, to augment curren
241 sing pathway including the von Hippel-Lindau tumor suppressor protein (pVHL) and the hypoxia inducibl
242 endent and -independent functions of the VHL tumor suppressor protein (pVHL) can contribute to tumor
243 tered metabolism in cancer cells related to: tumor suppressor protein (pVHL) function, the histone ac
244 ) have inactivation of the von Hippel-Lindau tumor suppressor protein (pVHL), resulting in the accumu
246 oded proteins with cell cycle regulators and tumor suppressor proteins, raising the possibility that
249 pment of liver cancer is a neutralization of tumor suppressor proteins Rb, p53, hepatocyte nuclear fa
250 romote phosphorylation of the retinoblastoma tumor suppressor protein (Rb) and other substrates.
254 control, Cdks inactivate the retinoblastoma tumor suppressor protein (Rb) through phosphorylation, w
256 N-terminal domain of the retinoblastoma (Rb) tumor suppressor protein (RbN) harbors in-frame exon del
257 biopsies showed nuclear accumulation of key tumor-suppressor proteins, reduction of cell proliferati
261 C-terminal domain (RbC) is necessary for the tumor suppressor protein's activities in growth suppress
267 st cancer susceptibility gene 1 (BRCA1) is a tumor suppressor protein that functions to maintain geno
270 AM and SH3 domain-containing protein 1) is a tumor suppressor protein that has roles in key cellular
271 on-associated miRNA-mediated regulation of a tumor suppressor protein that has the ability to influen
274 lysine 63 deubiquitinase gene (CYLD) encodes tumor suppressor protein that is mutated in familial cyl
276 bunit of an SCF ubiquitin ligase and a major tumor-suppressor protein that is altered in several huma
277 homolog deleted on chromosome 10 (PTEN) is a tumor-suppressor protein that regulates phosphatidylinos
278 though RASSF1A is now considered a bona fide tumor suppressor protein, the role of MOAP-1 as a tumor
279 proteins and host cell cycle regulators and tumor suppressor proteins, the relevance of these observ
280 Small molecule mediated stabilization of p53 tumor suppressor protein through sumoylation is a promis
281 method showed that translocation of the p53 tumor-suppressor protein to the perinucleus in immortali
282 By providing a means to restore a functional tumor-suppressor protein to tumor cells, PTEN-Long may h
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 SMARCB1 has also been recognized to be a tumor suppressor protein which controls many tumorigenic
293 residues creates binding sites for the COP1 tumor suppressor protein, which is an ubiquitin ligase c
294 f cancers with defects in the BRCA1 or BRCA2 tumor suppressor proteins, which are involved in the rep
299 ortance of FAK following deletion of the Apc tumor suppressor protein within the intestinal epitheliu
300 9 locus harbors an imprinted gene encoding a tumor suppressor protein within the long-sought WT2 locu