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1 l cancers, reflecting its critical role as a tumor suppressor.
2 gesting that CCAR2 may in fact function as a tumor suppressor.
3 receptor (IGF1R), functioning as a candidate tumor suppressor.
4 d MYC-dependent degradation of the p27(kip1) tumor suppressor.
5 tant mechanism by which SIRT6 functions as a tumor suppressor.
6 tuin-1, and beta-klotho, which can acts as a tumor suppressor.
7 rentiation and was shown to have a role as a tumor suppressor.
8  UL97 phosphorylates the retinoblastoma (Rb) tumor suppressor.
9 A miR-504 targets TP53 mRNA encoding the p53 tumor suppressor.
10 -mesencyhmal transition, thereby acting as a tumor suppressor.
11 ual role, acting either as a mitogen or as a tumor suppressor.
12 or CASZ1 to function as a neuroblastoma (NB) tumor suppressor.
13 ing motif that mimics the binding of the p53 tumor suppressor.
14 mors, also implicates Importin-11 as a novel tumor suppressor.
15 scription factor postulated to function as a tumor suppressor.
16 es MDM2 protein, which in turn degrades TP53 tumor suppressor.
17  was dependent on its interaction with BRCA1 tumor suppressor.
18 actor 6 (KLF6) is a transcription factor and tumor suppressor.
19  these negative Rac regulators solely act as tumor suppressors.
20 he high level of DNA methylation of putative tumor suppressors.
21 dditional mutational processes affecting key tumor suppressors.
22 signed for the discovery of Pten-cooperating tumor suppressors.
23 gene expression that can act as oncogenes or tumor suppressors.
24 re small GTPases that bind SmgGDS and act as tumor suppressors.
25 of the most up-regulated genes in CC was the tumor suppressor 15-PGDH/HPGD, and the most up-regulated
26 stinal stem cell marker, is known to exhibit tumor suppressor activity in colon cancer, the mechanism
27 ient and control tumors suggests that TRIM14 tumor suppressor activity may depend on cell death signa
28              The target genes mediating this tumor suppressor activity were unknown.
29  of DLC1 with focal adhesions and attenuates tumor suppressor activity.
30 neity, a function that may contribute to its tumor suppressor activity.
31  associated with activation of the metabolic tumor suppressor AMPKalpha1/2-LKB1, and a reduction in m
32  uncover a role in senescence for the potent tumor suppressor and ATM substrate USP28.
33 in turn, facilitates the accumulation of the tumor suppressor and HR effector BRCA1 at replication fo
34 ate that MRN cannot be considered a standard tumor suppressor and instead imply that nuclease activit
35 tin ligase, is a potent inhibitor of the p53 tumor suppressor and is elevated in many human cancers t
36 ted factor 2 (EAF2) is an androgen-regulated tumor suppressor and its intracellular localization can
37                                              Tumor suppressor and upstream master kinase Liver kinase
38 rs, the caspases, have long been regarded as tumor suppressors and one hallmark of cancer is 'Evading
39                        Further, we find that tumor-suppressor and oncogenic mutant BAF complexes have
40 a increasing the expression of E-cadherin, a tumor suppressor, and decreasing the expression of mesen
41 , demonstrate that MCSC quiescence acts as a tumor suppressor, and identify the extrinsic environment
42                               IRF5 is also a tumor suppressor, and its expression is dysregulated in
43                                 One third of tumor suppressors are haploinsufficient transcriptional
44 pecific genetic alterations in oncogenes and tumor suppressors are highly context-dependent and are p
45 s, coupled with inactivation of the INK4/ARF tumor suppressors, are hallmarks of T-lineage acute lymp
46 dies have identified a critical role for the tumor suppressors BRCA1 and BRCA2 in preventing the degr
47                             Mutations in the tumor suppressor BRCA2 predominantly predispose to breas
48 es its role in homologous recombination, the tumor suppressor BRCA2 protects stalled replication fork
49 ability to recognize RPA-coated ssDNA to the tumor suppressor BRCA2, which is complexed with RAD51.
50    Mutations truncating a single copy of the tumor suppressor, BRCA2, cause cancer susceptibility.
51 romyelocytic leukemia (PML) is a pleiotropic tumor suppressor, but its role in tumor microenvironment
52 umulating evidence suggests that Parkin is a tumor suppressor, but the underlying mechanism is poorly
53 ted that it can serve as an immune-dependent tumor suppressor by acting as a chemoattractant to recru
54                 Nuclear FOXO proteins act as tumor suppressors by transcriptionally activating genes
55 rted that p53 protein, although a well-known tumor suppressor, can contribute to cancer cell survival
56 c effect of the KRAS or EGFR driver and TP53 tumor suppressor comutation.
57  pathway in the colon epithelium, where FoxO tumor suppressors could provide protection from redox st
58                                     Although tumor suppressor CtIP is critical for DSB end resection,
59 KT1 activation by binding and inhibiting the tumor suppressor DAB2IP (DAB2-interacting protein) in th
60 opmental defects in mutants of the conserved tumor suppressor death-associated protein kinase dapk-1
61 targets were actin regulators, including the tumor suppressor eplin.
62 dentify putative 'escape from X-inactivation tumor-suppressor' (EXITS) genes, we examined somatic alt
63 e a regulatory network that involves the p53 tumor suppressor family and the Wnt pathway acting toget
64 Thus our study identifies RARRES2 as a novel tumor suppressor for ACC, which can function through an
65           Although generally considered as a tumor suppressor, FOXO1 is consistently upregulated in t
66   The multispecific transcription factor and tumor suppressor FOXO3 is an important mediator of apopt
67 ations of FBW7, an E3 ubiquitin ligase and a tumor suppressor frequently mutated in CRCs, contribute
68              These latter findings support a tumor suppressor function for KIND1, and identify c-Jun
69                        Our results suggest a tumor suppressor function for SIN3B that limits prostate
70  leukemia.Significance: This study defines a tumor suppressor function for the protein tyrosine phosp
71 come legitimate concerns associated with the tumor suppressor function of nontargeted Notch pathway i
72          Four of the six BDs abrogated PBRM1 tumor suppressor function, gene regulation, and chromati
73 mber of p53 target genes, which confer p53's tumor suppressor function, has led to increasingly compl
74  knockdown of GRM3 enhances TGFbeta-mediated tumor suppressor function.
75 nserved gene pathways associated with Ikaros tumor suppressor function.
76  protein stability of HIPK2 and enhances its tumor suppressor function.
77 barcode sequencing (Tuba-seq) to interrogate tumor-suppressor function in mouse models of human cance
78 ncer-mediated gene regulation as a principal tumor-suppressor function of ARID1A.
79  of RUNX1, a transcription factor with known tumor-suppressor function.
80 vation in PMAH suggested that ARMC5 may have tumor suppressor functions in the adrenal cortex.
81                However, the mechanism of the tumor suppressor functions of E2F7/8 remain obscure.
82 (HR), the molecular mechanism underlying the tumor suppressor functions of FANCJ remains obscure.
83 ent cellular contexts, such as oncogenic and tumor-suppressor functions and hematopoietic and cardiac
84 ghts into its control and into the suggested tumor-suppressor functions of Smurf2.
85 tor erythroid 2-related factor 2 (Nrf2), and tumor suppressor gene (p53) when children or adults were
86 cs, we have found that KANK1 was a candidate tumor suppressor gene (TSG) for human MPNSTs.
87 f its phosphorylated state mediated by large tumor suppressor gene 1 and 2 (LATS1/2).
88 (IR) induces the expression of p16(INK4a), a tumor suppressor gene and senescence/aging biomarker.
89  confirmed that miR-210 directly targets the tumor suppressor gene APC (adenomatous polyposis coli),
90     However, little is known about whether a tumor suppressor gene can function through both immune-d
91 heterozygous missense mutations in SAMD9L, a tumor suppressor gene located on chromosome arm 7q.
92 moresistance caused by downregulation of the tumor suppressor gene miR-34a.
93 on disorder due to germline mutations in the tumor suppressor gene NF1.
94 ealed recurrent somatic inactivations of the tumor suppressor gene Ptch1 and a recapitulation of the
95 ic translation initiation factor EIF4A1, the tumor suppressor gene PTEN and the long non-coding RNA N
96 has shown that miRNA-based regulation of the tumor suppressor gene PTEN can be modulated by the expre
97                                  Loss of the tumor suppressor gene PTEN exerts diverse outcomes on ca
98 d breaks (DSB) in cancer cells that lack the tumor suppressor gene RUNX3 Loss of RUNX3 resulted in tr
99 stribution, differential gene expression and tumor suppressor gene status.
100            Mutations at CpG sites on the p53 tumor suppressor gene that can result from these adducti
101 lls deficient in the von Hippel-Lindau (VHL) tumor suppressor gene use glutamine to generate citrate
102 he results suggest that VGLL4 is a candidate tumor suppressor gene which acts by selectively antagoni
103 METTL7A (Methyltransferase Like 7A), a novel tumor suppressor gene with multiple editing sites at its
104 n function as a traditional loss-of-function tumor suppressor gene, and they provide a fully penetran
105 ssion of both the RAD52 gene, and the HR and tumor suppressor gene, BRCA2, in human cells synergistic
106 e evidence for PPP2R4 as a haploinsufficient tumor suppressor gene, defining a high-penetrance geneti
107 rapeutic-ultrasound (TUS) to deliver a human tumor suppressor gene, hSef-b, to prostate tumors in viv
108  fragments of menin, the product of the MEN1 tumor suppressor gene, in coordinating the transcription
109     Caused by a germline mutation in the NF1 tumor suppressor gene, individuals with NF1 are prone to
110  MPSNTs are associated with mutations in NF1 tumor suppressor gene, resulting in activation of Ras an
111 ic cancers, as widely documented for the p53 tumor suppressor gene.
112 luded those predicted to target oncogenes or tumor suppressor gene.
113 STAiR2 originates from the first intron of a tumor suppressor gene.
114 st identified in Peutz-Jeghers syndrome as a tumor suppressor gene.
115 one possible explanation why Parkin may be a tumor suppressor gene.
116 initiated by somatic inactivation of the VHL tumor suppressor gene.
117  This discovery uncovers novel mechanisms of tumor-suppressor gene inactivation and highlights a new
118 in human retinoblastoma are mutations in the tumor-suppressor gene retinoblastoma (RB) and amplificat
119 rosis complex (TSC) is an autosomal dominant tumor-suppressor gene syndrome caused by inactivating mu
120 l into two broad categories: inactivation of tumor suppressor genes (hypomorph, antimorph or amorph)
121  were able to simultaneously inactivate five tumor suppressor genes (TP53, PTEN, APC, BRCA1, and BRCA
122 orphic mutations, which can be found in both tumor suppressor genes and oncogenes, produce proteins w
123                                              Tumor suppressor genes and the immune system are critica
124 ions in the tuberous sclerosis complex (TSC) tumor suppressor genes are associated closely with the p
125 ead to the replacement of single, functional tumor suppressor genes by the mutant alleles.
126                           Thus, mutations in tumor suppressor genes can create a state of increased c
127 ISPR-Cas9-based editing of the Apc and Trp53 tumor suppressor genes in colon epithelial cells and by
128 our screens in multiple cancer types, as new tumor suppressor genes in prostate cancer.
129         We observed that hypermethylation of tumor suppressor genes is a frequent event in ocular tum
130 Aberrant DNA hypermethylation of promoter of tumor suppressor genes is commonly observed in cancer, a
131 thogenesis of cancer either by silencing key tumor suppressor genes or by activating oncogenes.
132 lso reprogram several hypoxia associated and tumor suppressor genes such as MAT2A and PDK-1, in addit
133 , such as kidney cells with mutations in the tumor suppressor genes tuberous sclerosis complex (TSC)1
134                          Known oncogenes and tumor suppressor genes, beyond those engineered, are mut
135 stability that, in the absence of functional tumor suppressor genes, can contribute to tumorigenesis.
136 thylation (H3K27me3), and (ii) activation of tumor suppressor genes, including BRCA1.
137 pression and increased expression of several tumor suppressor genes, including Src homology region 2
138 ed in G1-S phase arrest and act as potential tumor suppressor genes, we aimed to study potential meth
139 -of-function mutations of the PBRM1 and BAP1 tumor suppressor genes, which occur in a mutually exclus
140 ation with cancer-associated genes including tumor suppressor genes.
141 , some of which are associated with putative tumor suppressor genes.
142 urrently mutated, and the identity of key 8p tumor-suppressor genes (TSG) is unknown.
143 and heterogeneous carcinoma in which various tumor-suppressor genes are lost by mutation, deletion, o
144                           Comutated, myeloid tumor-suppressor genes contribute to phenotypic variabil
145 ive prostate cancers, which retain potential tumor-suppressor genes in the interstitial regions betwe
146  implicated in human melanoma, including the tumor-suppressor genes phosphatase and tensin homolog (P
147  that activate proto-oncogenes or inactivate tumor-suppressor genes.
148 heir breakpoints and recurrently inactivated tumor-suppressor genes.
149 llele-specific overexpression of variants in tumor-suppressor genes.
150                                              Tumor suppressor helps reprogram Schwann cells to promot
151 tumor growth in vivo EPI and NE activate the tumor suppressor Hippo signaling pathway, and the suppre
152                The protein expression of the tumor suppressor HNF4alpha may be inhibited by interacti
153                                          The tumor suppressors ID3, ARID1A, APC, and CDKN2A are frequ
154                                    PAX5 is a tumor suppressor in B-ALL, while the role of PAX5 fusion
155 ll, our studies reveal miR-424(322)/503 as a tumor suppressor in breast cancer and provide a link bet
156              PDZK1 was identified as a novel tumor suppressor in ccRCC by negating SHP-1 activity.
157 he K(+) channel KCNQ1 has been proposed as a tumor suppressor in colorectal cancer (CRC).
158 ipids that has been recently identified as a tumor suppressor in colorectal cancer, yet its potential
159 thylcytosine dioxygenase that functions as a tumor suppressor in hematopoietic malignancies.
160 results suggest that KANK1 may function as a tumor suppressor in human MPNSTs, and thus it may be use
161                            p53 is a critical tumor suppressor in humans.
162 ing protein INO80C was identified as a novel tumor suppressor in KRAS(MUT) colorectal and pancreatic
163  controlling myelopoiesis and is a potential tumor suppressor in leukemia.
164 In summary, miR-193b not only functions as a tumor suppressor in liposarcoma but also promotes adipog
165 ex member loss, identifies Setd2 as a potent tumor suppressor in lung adenocarcinoma, and establishes
166 ltransferase, which has been implicated as a tumor suppressor in mammals.
167 ignaling and has been shown to function as a tumor suppressor in multiple cancer types.
168            Recently, SEMA3B has emerged as a tumor suppressor in non-neuronal cells.
169 ogene in some cellular backgrounds, and as a tumor suppressor in others, and the molecular mechanism
170 vide evidence that ABHD5 acts as a metabolic tumor suppressor in PCa that prevents EMT and the Warbur
171 he mechanisms by which Ikaros functions as a tumor suppressor in pre-B ALL remain poorly understood.
172 otch receptor paralogs cooperate to act as a tumor suppressor in squamous cell carcinomas (SCCs).
173 y complex serves as a previously undescribed tumor suppressor in the liver, restraining TNFR1-indepen
174 re we demonstrate that Arid1a functions as a tumor suppressor in the mouse colon, but not the small i
175 Foxp1, cooperated with loss of the Cdkna2a/b tumor suppressors in promoting B-ALL development.
176 nly down-regulated transcription factors and tumor suppressors in renal cell cancer (RCC).
177      Expression of many oncogenes or loss of tumor suppressors induces the expression of immune check
178 '-like condition and transform caspases from tumor suppressors into tumor promotors.
179                                      The p53 tumor suppressor is a pivotal guardian of genomic stabil
180 tion of the adenomatous polyposis coli (APC) tumor suppressor is frequently found in colorectal cance
181                           In these mice, the tumor suppressor isoform of CUGBP1 is protected from Gan
182      Germline mutations in the gene encoding tumor suppressor kinase LKB1 lead to gastrointestinal tu
183 e, BITC-induced p53 and p73 axes converge on tumor-suppressor LKB1 which is transcriptionally upregul
184 ed in multiple types of cancer and acts as a tumor suppressor lncRNA by reducing the invasive phenoty
185 Thus, our data introduce the IPO11 gene as a tumor-suppressor locus, which is of special importance i
186 ependent growth in the context of concurrent tumor suppressor loss.
187 nd BCL6) downstream of common oncogenes, and tumor suppressors may provide a potent way to defeat int
188 ed senescence (OIS) is considered a powerful tumor suppressor mechanism.
189                              MiR-34a acts as tumor suppressor microRNA (miRNA) in several cancers, in
190 lative influence for 15,798 genes, including tumor suppressor, mitochondrial, and mismatch repair gen
191 tudies demonstrate that atypical E2Fs act as tumor suppressors, most likely via transcriptional repre
192 ur study identified complex PTEN-cooperating tumor suppressor networks in different cancer types, wit
193                          Inactivation of the tumor suppressor neurofibromin 1 (NF1) presents a newly
194 tural protein (NS) 5B, directly binds to the tumor suppressor, NORE1A (RASSF5), and promotes its prot
195 18 gene has been proposed to act either as a tumor suppressor or as an oncogene in different human ca
196 sformation and/or tumorigenesis, as either a tumor suppressor or tumor promoter, is complex and may b
197  that has been demonstrated to function as a tumor suppressor or, conversely, as an oncogene in a con
198          Here we show that expression of the tumor suppressor p14(ARF) (ARF) is upregulated in aggres
199   Our studies reveal, intriguingly, that the tumor suppressor p14ARF binds to this segment and may th
200  hypomethylation, restores the expression of tumor suppressor p15(INK4B) through promoter demethylati
201                                          The tumor suppressor P19(ARF) is strongly activated in the n
202                                  Loss of the tumor suppressor p53 (encoded by TP53) provides cancer c
203 3), a common stress sensor, can activate the tumor suppressor p53 and regulate expression of p53 targ
204                  Human TP53 gene encodes the tumor suppressor p53 and, via alternative splicing, the
205             We address this question for the tumor suppressor p53 by combining live-cell single-molec
206 tency and its related cancers.IMPORTANCE The tumor suppressor p53 is a critical cellular protein in r
207                                          The tumor suppressor p53 is a well-characterized transcripti
208                                          The tumor suppressor p53 is widely dysregulated in cancer an
209                             Mutations in the tumor suppressor p53 occur in a majority of human cancer
210                                              Tumor suppressor p53 plays a central role in tumor suppr
211 ymphocytes in vitro and possibly in vivo The tumor suppressor p53 plays a seminal role in cancer deve
212                Many oncogenic mutants of the tumor suppressor p53 rapidly aggregate but form amorphou
213                                 Mutations in tumor suppressor p53 remain a vital mechanism of tumor e
214 ubiquitinase implicated in destabilizing the tumor suppressor p53, and for this reason it has gained
215 ria, mediate downstream apoptotic effects of tumor suppressor P53, and inhibit the antioxidant respon
216  cancer stem cells (CSCs) by suppressing the tumor suppressor p53.
217 creatic tumors or changing the status of the tumor suppressors p53, p16(Ink4a) and p19(Arf).
218  The two BRCA proteins are linked by a third tumor suppressor, PALB2, in the HR pathway.
219                                    The Hippo tumor suppressor pathway is essential for development an
220 the pivotal MOB1 signal transducer.The Hippo tumor suppressor pathway is essential for development an
221           The core LATS kinases of the Hippo tumor suppressor pathway phosphorylate and inhibit the d
222        Disruption of the retinoblastoma (RB) tumor suppressor pathway, either through genetic mutatio
223 % of HCCs are clonal, with alteration of key tumor-suppressor pathways in stem cells as the primary c
224 d to sustain cancer cell growth in which the tumor suppressor phosphatase and tensin homolog (PTEN) h
225  study, we have found that expression of the tumor suppressor, phosphatase and tensin homolog deleted
226 regulates EZH2, leading to inactivation of a tumor suppressor program in neuroblastoma, and support t
227 gulatory noncoding elements and uncovers the tumor-suppressor properties of ACTRT1.
228 asmic dynein, the adenomatous polyposis coli tumor suppressor protein (APC), and glycogen synthase ki
229 of Cdc25A led to reduction in retinoblastoma tumor suppressor protein (pRb) phosphorylation.
230                       Here, we show that the tumor suppressor protein adenomatous polyposis coli (APC
231 resents evidence that de-ph-S302-CUGBP1 is a tumor suppressor protein and that the Gank-UPS-mediated
232 ell, Chen et al. (2017) demonstrate that the tumor suppressor protein ARF sensitizes cancer cells to
233                                          The tumor suppressor protein Merlin is proteasomally degrade
234                                          The tumor suppressor protein p53 acts as a transcription fac
235                          Inactivation of the tumor suppressor protein p53 by mutagenesis, chemical mo
236        Under normal cellular conditions, the tumor suppressor protein p53 is kept at low levels in pa
237                                          The tumor suppressor protein p53, the "guardian of the genom
238                                      The p53 tumor suppressor protein plays a critical role in orches
239 ast cancer by showing how it upregulates the tumor suppressor protein PML.
240                                          The tumor suppressor protein retinoblastoma (RB) is mechanis
241 e for the cyclin D1/Cdk4/pRb (retinoblastoma tumor suppressor protein) pathway in delayed neuronal de
242 ased HIF-1alpha binding to von Hippel-Lindau tumor suppressor protein, an E3 ligase component and an
243                        We found induction of tumor suppressor protein, p53, and apoptosis with suppre
244  a significant role in the regulation of the tumor suppressor protein.
245 the functionally critical UCH domain in this tumor suppressor protein.
246 s, and binding of inhibitors such as the p27 tumor suppressor protein.
247                          p53 is an important tumor-suppressor protein deactivation of which by mdm2 r
248                            Menin (MEN1) is a tumor-suppressor protein in neuroendocrine tissue.
249 bunit of an SCF ubiquitin ligase and a major tumor-suppressor protein that is altered in several huma
250           In contrast, CYLD (cylindromatosis tumor-suppressor protein), a K63-specific deubiquitinase
251 s the key mediator of nuclear export of many tumor suppressor proteins and is overexpressed in human
252 wth, was remarkably downregulated, while the tumor suppressor proteins p53 and p21 were substantially
253 ) function, leads to nuclear accumulation of tumor suppressor proteins, and induces cancer cell death
254  development of small molecule activators of tumor suppressor proteins.
255                                          The tumor suppressor PTEN controls cell proliferation by reg
256 en et al. show that Importin-11 traffics the tumor suppressor PTEN into the nucleus and in so doing p
257              Dictyostelium cells lacking the tumor suppressor PTEN show strongly impaired migratory a
258  aeruginosa clearance through activating the tumor suppressor PTEN.
259  miR-221/222 in regulating expression of the tumor suppressor PTEN.
260                                  Loss of the tumor suppressors RB1 and TP53 and MYC amplification are
261 ce deficient for Trp53, we confirm that this tumor suppressor regulates NK cell functional maturation
262 ators and function as a proto-oncogene and a tumor suppressor respectively in human oncogenesis.
263                                          p53 tumor suppressor responds to various cellular stresses a
264 eins activate the PI3K/AKT pathway and evade tumor suppressor responses.
265 Loss of the tuberous sclerosis complex (TSC) tumor suppressors results in activation of mTORC1 and de
266                      Our results establish a tumor suppressor role for PTP1B in the myeloid lineage c
267                           Our results show a tumor suppressor role of AKT-phosphorylated FOXO1 in the
268 ata suggest a retinoic acid-independent, non-tumor suppressor role of CRABP2 for the survival of MPNS
269         Therefore, our results elucidate the tumor-suppressor role of SPOP in prostate cancer in whic
270              RUNX1 has been proposed to have tumor suppressor roles in T-cell leukemia homeobox 1/3-t
271 trate that gain-of-function mutations in the tumor suppressor SAMD9L cause cytopenia, immunodeficienc
272                                          The tumor suppressor serine/threonine kinase 11 (LKB1/STK11)
273           Overall, our findings show how the tumor suppressor SIRT6 is regulated in hepatocellular ca
274 on and degradation of wild-type SS18 and the tumor suppressor SMARCB1.
275                       Alterations in the VHL tumor suppressor stabilizing the hypoxia-inducible facto
276 lls carrying mutations in the major emerging tumor suppressor STAG2 across different cancer contexts.
277 mutations are from four genes, including two tumor suppressors (TGFBR1 and CHEK2) and two oncogenes (
278  Interferon regulatory factor 1 (IRF-1) is a tumor suppressor that is also involved in the regulation
279                               P53 is a major tumor suppressor that is mutated and inactivated in 50%
280 d inactivating the retinoblastoma protein, a tumor suppressor that restrains G1- to S-phase progressi
281                                 Unlike other tumor suppressors that are frequently deleted or acquire
282        The switch converting TGF-beta from a tumor-suppressor to tumor-promoter has not been identifi
283                                          The tumor suppressor TP53 is the most frequently mutated gen
284                                          The tumor suppressor Trp53 (p53) inhibits cell growth after
285 genes ADNP, AP2B1, TOMM70A and ZNF326 showed tumor suppressor (TS) activity in tumor xenograft studie
286  genetic screen to identify and validate new tumor suppressors (TS) in this disease.
287                                          The tumor suppressors Tsc1 and Tsc2 form the tuberous sclero
288 S/L interactions with TSC1 and TSC2, the two tumor suppressors underlying tuberous sclerosis complex
289 onditional deletion of the von Hippel-Lindau tumor suppressor (VHL) protein in the forkhead box FOXD1
290 owed that Mig-6 has an important function of tumor suppressor via inhibition of STAT3 phosphorylation
291                        The hypoxia-regulated tumor-suppressor von Hippel-Lindau (VHL) is an E3 ligase
292 ent in many cancer types, TGF-beta acts as a tumor suppressor, whereas in the advanced stages of thes
293  shows that HSulf-1 (endosulfatase), a known tumor suppressor which attenuates heparin sulfate bindin
294     TFPI-2 has recently been recognized as a tumor suppressor, which not only plays a fundamental rol
295  kinase B1) is a serine/threonine kinase and tumor suppressor, which regulates the homeostasis of hem
296 loss of the tuberous sclerosis complex (TSC) tumor suppressors, which exhibit growth factor-independe
297 ation therapy designed to reactivate the p53 tumor suppressor while antagonizing the anti-apoptotic f
298 e p53(53,54) TAD2 mutant behaves as a "super-tumor suppressor," with an enhanced capacity to both sup
299 red predominantly within the human and mouse tumor suppressor WW Domain Containing Oxidoreductase (WW
300 ulates hepatic metabolism and functions as a tumor suppressor, yet systematic and direct biochemical

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