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1 ative transcription factor may also act as a proto-oncogene.
2 emia through aberrant expression of the EVI1 proto-oncogene.
3 F2alpha regulation is JNK dependent, via jun proto-oncogene.
4 lowing for quantitative analysis of the cMYC proto-oncogene.
5 inhibitors, and overexpression of the c-Myc proto-oncogene.
6 the estrogen receptor coregulator PELP1 is a proto-oncogene.
7 has previously been described as a powerful proto-oncogene.
8 r and therefore generally considered to be a proto-oncogene.
9 t into the categorization of ECT2 as a human proto-oncogene.
10 ss mRNAs including the mRNA encoding the Mos proto-oncogene.
11 he translocation and the deregulation of the proto-oncogene.
12 quently associated with mutations to the RET proto-oncogene.
13 cations between a tissue-specific gene and a proto-oncogene.
14 s a member of Fos gene family and is a known proto-oncogene.
15 oglobulin heavy-chain transcription and as a proto-oncogene.
16 n epidermal growth factor receptor 2 [HER2]) proto-oncogene.
17 r the transcriptional expression of the cMet proto-oncogene.
18 by the activated oncogene compared with the proto-oncogene.
19 ose expression mimics that of the nearby MYC proto-oncogene.
20 ssor genes, restrict the activity of the Src proto-oncogene.
21 isk region physically interacts with the MYC proto-oncogene.
22 ene homolog (Kras), or overexpression of MYC proto-oncogene.
23 h splicing factor 3 (SRSF3 or SRp20) being a proto-oncogene.
24 gulation, like P53 tumor suppressor and cMYC proto-oncogene.
25 GCM2, suggesting that GCM2 is a parathyroid proto-oncogene.
26 in the rearranged during transfection (RET) proto-oncogene.
27 ain of specific genomic loci known to harbor proto-oncogenes.
28 activate tumor suppressor genes and activate proto-oncogenes.
29 factor activity of the NOTCH1, MYC, and IRF4 proto-oncogenes.
30 k of transcription factors including several proto-oncogenes.
31 owths due to vector insertion near or within proto-oncogenes.
32 onmalignant cells was sufficient to activate proto-oncogenes.
33 ted neighborhoods containing prominent T-ALL proto-oncogenes.
34 druplex structures are found in promoters of proto-oncogenes.
36 e closely linked E26 transformation-specific proto-oncogene 1 (ETS1) is overexpressed in these FLI1-d
37 stic lymphoma kinase (ALK)-rearranged or ROS proto-oncogene 1 (ROS1)-rearranged non-small-cell lung c
38 h pathways dependent or not dependent on ABL proto-oncogene 1 non-receptor tyrosine kinase (c-Abl).
39 ncided with a 4.5-fold increase in ETS1 (ETS proto-oncogene 1) mRNA, suggesting that ETS1 is involved
40 tibody and a breakpoint cluster region - ABL proto-oncogene 1, nonreceptor tyrosine kinase (BCR-ABL1)
43 gammaretrovirus vectors have caused cellular proto-oncogene activation and leukemia, necessitating th
44 om an index patient and demonstrate that MET proto-oncogene activation is important for tumor growth
46 tidyl inositol 3 kinase (PI3K)-thymoma viral proto-oncogene (AKT) inhibitors to kill tumor cells.
47 regulated kinase (ERK) and the thymoma viral proto-oncogene (Akt), followed by activation of the mamm
48 ocess that we hypothesized involved c-met, a proto-oncogene amplified in breast tumors that promotes
49 ts in this tumour, including one in the KRAS proto-oncogene and 391 others in coding regions, as well
50 are cell cycle regulators and function as a proto-oncogene and a tumor suppressor respectively in hu
51 e multifunctional signal transducer Ras is a proto-oncogene and frequently becomes mutated in a varie
53 The Skp2 E3-ubiquitin ligase can act as a proto-oncogene and its aberrant overexpression is freque
54 esults therefore identify miR-22 as a potent proto-oncogene and suggest that aberrations in the miR-2
55 is study shows that Erk1 can be considered a proto-oncogene and that Erk molecules possess unusual au
57 Ecotropic viral integration site 1 (EVI1), a proto-oncogene and zinc finger transcription factor, pla
58 ed by numerous common integration sites near proto-oncogenes and by increased abundance of clones wit
60 scription factor genes, including MYC family proto-oncogenes and neuroendocrine lineage-specific fact
61 e p53 mutations or undergo amplifications of proto-oncogenes and receptor tyrosine kinases, implicati
62 n-protein interactions, including binding to proto-oncogenes and tumor suppressors to regulate cell d
65 tor of activated T cells 3 (NFATc3) and FosB proto-oncogene, AP-1 transcription factor subunit (FosB)
67 to constitutive activation of NRAS and KRAS proto-oncogenes are among the most common in human cance
71 directly activated the transcription of the proto-oncogene BCL6 in normal germinal-center (GC) B cel
72 core Sgamma1 region into the first intron of proto-oncogene Bcl6, which is a non-Ig target of SHM.
73 und that a key transcriptional repressor and proto-oncogene, Bcl6 is significantly down-regulated in
74 ng is often considered a model hematopoietic proto-oncogene because of its role as the main trigger o
76 isms that prevent proteasomal degradation of proto-oncogene beta-catenin (CTNNB1) and its eventual tr
77 s the Wnt-signaling pathway by targeting the proto-oncogene beta-catenin for destruction by cytoplasm
79 ing pathway, directed by the oncogenic B-Raf proto-oncogene (BRAF) variant BRAF(V600E), that mediates
80 y displays mutational activation of the KRAS proto-oncogene but, unlike lung cancers expressing mutat
81 shown to be negatively modulated by the MYCN proto-oncogene, but the mechanism of repression was uncl
82 , activation of otherwise normally repressed proto-oncogenes by promoter demethylation has been infre
83 d ATM-dependent signalling, and identify the proto-oncogene c-Abl as a mediator of this modification.
85 e shown that co-expression of TAp73 with the proto-oncogene c-Jun can augment cellular growth and pot
86 rrelation between GAPDH upregulation and the proto-oncogene c-jun expression (r = 0.543, P = .003).
89 ivity requires binding to its receptors, the proto-oncogene c-Met and heparan sulfate proteoglycan (H
90 oticed transcriptional repression of 5-LO by proto-oncogene c-Myb and conclude that loss of stromal 5
91 egulated at the transcriptional level by the proto-oncogene c-Myb and is required for c-Myb-induced p
93 blocked at the polymorphic site and that the proto-oncogene c-MYB modulates the release of the pausin
95 reconstructed in cell culture, and that the proto-oncogene c-Myc controls the generation of self-ren
97 We have previously demonstrated that the proto-oncogene c-Myc is essential for all the phenotypes
103 MR) status and somatic mutation in the B-Raf proto-oncogene (c.1799T>A [V600E]; BRAFV600E) or exon 2
106 ve established that amplification of the MET proto-oncogene can cause resistance to epidermal growth
107 Numerous kinase pathways and products of proto-oncogenes can up-regulate Pol I, whereas tumor sup
111 viral vectors, but insertional activation of proto-oncogenes contributed to leukemia in some patients
112 ied novel direct targets, including CRK-like proto-oncogene (CRKL) and focal adhesion kinase (FAK).
114 sion in association with mRNAs encoding many proto-oncogenes, cytokines, chemokines, and proinflammat
116 e runt-related transcription factor 1, Fli-1 proto-oncogene, E-twenty-six (ETS) transcription factor
117 PTTG1-dependent expression of the RhoGEF proto-oncogene ECT2 was observed in a number of ccRCC ce
120 The RET (rearranged during transfection) proto-oncogene encodes a receptor tyrosine kinase for me
128 showed that miR-155 is coexpressed with the proto-oncogene encoding c-MYC in positively selected B c
129 mammary carcinoma cells that overexpress the proto-oncogene Erbb2 (also known as Neu), which is frequ
132 human androgen receptor (AR) coactivator and proto-oncogene expressed at low levels in normal human r
135 this method by examining copy number in the proto-oncogene FLT3 and the common V600E point mutation
136 e resulted in an increased expression of the proto-oncogenes FOS and JUN in both cell lines at 72 hr.
137 rough a series of studies, we identified the proto-oncogene fosab (cfos) as a potent miR-101a target
145 cellular apoptosis; we also showed that the proto-oncogene H-Ras becomes activated in these cells un
148 e discovery of potent inhibitors of the BRAF proto-oncogene has revolutionized therapy for melanoma h
149 direct pharmacological inhibition of the RAS proto-oncogene has thus far been unsuccessful, we explor
150 binger DNA transposons carrying the Myb-like proto-oncogene have expanded dramatically in the Pleurod
151 miR-221 and miR-222, upregulated by the MET proto-oncogene, have been already described to enhance c
154 nvadopodia component Tks5long, the embryonal proto-oncogene Hmga2, and the epithelial-to-mesenchymal
155 xpression of the shorter mRNA isoform of the proto-oncogene IGF2BP1/IMP-1 led to far more oncogenic t
157 nslation of the mixed lineage leukemia (MLL) proto-oncogene in an arginine methylation-dependent mann
160 eased copy number and expression of the PIM1 proto-oncogene in genomic data sets of patients with TNB
161 a mechanism by which lncRNA MALAT1 acts as a proto-oncogene in hepatocellular carcinoma, modulating o
163 w mechanistic insights into the role of this proto-oncogene in stem cell differentiation, neuronal ag
164 Amplifications and mutations in the KIT proto-oncogene in subsets of melanomas provide therapeut
167 gs to the most frequent aberrantly expressed proto-oncogenes in human acute leukemias and is highly l
172 domain-containing 7 (Fbw7) degrades several proto-oncogenes including c-Myc, cyclinE, Notch1, and c-
173 d transcriptional activation of a network of proto-oncogenes, including Erg, Flt3, Lmo2, Myb, and Sox
176 r BRCA1-deficient MBC by introducing the MET proto-oncogene into a BRCA1-associated breast cancer mod
177 as originally identified as the product of a proto-oncogene involved in chromosomal translocations in
178 expression strongly correlates with c-jun, a proto-oncogene involved in liver tumorigenesis in human
182 Expression of the MECOM (also known as EVI1) proto-oncogene is deregulated by chromosomal translocati
185 mplification and overexpression of erbB2/neu proto-oncogene is observed in 20-30% human breast cancer
187 enome has recently disclosed that the NOTCH1 proto-oncogene is recurrently mutated at CLL presentatio
189 ell leukemia 1 (TCL1), the AKT modulator and proto-oncogene, is differentially expressed in CLL and l
191 the Drosophila homologue of the human c-myc proto-oncogene, is regulated in vitro and in vivo by mem
192 30 (involved in membrane transport), and the proto-oncogene JUN, indicate that the Rab1b increase act
193 e transcription factor c-Jun, product of the proto-oncogene JUN, is a key regulator of mitochondrial
194 ents FBJ osteosarcoma oncogene (FOS) and jun proto-oncogene (JUN) to the promoters of a subset of Tol
198 >A [V600E]; BRAFV600E) or exon 2 of the KRAS proto-oncogene (KRAS) in the primary tumor with SAR in p
199 mutations in the RET (formerly MEN2A, MEN2B) proto-oncogene located on chromosomal band 10q11.21.
200 rms a long-range chromatin loop with the MYC proto-oncogene located several hundred kilobases telomer
203 BBB permeability in part because Src kinase proto-oncogene members stimulate proliferation of newbor
204 signaling uses lateral activation of the met proto-oncogene (MET) through SRC proto-oncogene nonrecep
207 These include the signaling gene TGFBR1, the proto-oncogene MYB as well as many immune-related genes
209 strong, haplotype-specific activation of the proto-oncogene MYC by the integrated HPV-18 genome appro
217 ated ITG-dependent focal adhesion kinase/Src proto-oncogene non-receptor tyrosine kinase signaling.
219 of the met proto-oncogene (MET) through SRC proto-oncogene nonreceptor tyrosine kinase to maximize c
221 lated neighborhoods, we investigated whether proto-oncogenes occur within these structures and whethe
223 i-novel protein) was discovered as a nuclear proto-oncogene on the basis of its ability to induce tra
225 en initiated by genetic events that activate proto-oncogenes or inactivate tumor-suppressor genes.
226 a biophysical characterization of the c-MYC proto-oncogene P1 promoter quadruplex and its interactio
229 Here, we identify the protein kinase and proto-oncogene PIM3 as being repressed downstream of mTO
230 ayed highly significant up-regulation of the proto-oncogene pleomorphic adenoma gene 1 (PLAG1), sugge
231 ver, whether the human mTOR gene itself is a proto-oncogene possessing tumorigenicity has not been fi
232 guingly, YccA is a functional homolog of the proto-oncogene product Bax Inhibitor-1, which may share
234 SF) and its receptor, the product of the MET proto-oncogene, promote invasion and metastasis of tumor
235 pe was observed by overexpressing c-Myc (Myc proto-oncogene protein), a downstream target of Pim kina
237 el in Drosophila, oncogenic mutations of the proto-oncogene Ras (Ras(V12)) maintain tumorous cells in
238 wth factor (HGF) acting through its specific proto-oncogene receptor c-Met has been suggested to play
239 nfluences the prognostic significance of KIT proto-oncogene receptor tyrosine kinase (KIT) and platel
242 the identification of clients, such as Raf-1 proto-oncogene, Ser/Thr kinase (RAF1), that are particul
244 ard, which in turn gradually suppressed RAF1 proto-oncogene serine/threonine kinase (RAF1)/ERK signal
245 Here, we report the efficacy of the Raf proto-oncogene serine/threonine protein kinase (RAF) inh
246 ted HRAS(G12V) with its effector protein RAF proto-oncogene serine/threonine protein kinase 1 (RAF1).
247 inst unrelated protein kinases; however, the proto-oncogene serine/threonine protein kinase PIM1 (PIM
249 errant HGF-MET (hepatocyte growth factor-met proto-oncogene) signaling activation via interactions wi
251 variation in ten individuals with SGS in the proto-oncogene SKI, a known repressor of TGF-beta activi
252 bited antifibrotic Sloan-Kettering Institute proto-oncogene (Ski) and Ski-related novel gene, non-Alu
255 knockout technology, we disrupted the c-myb proto-oncogene specifically in adult bone marrow (BM) to
257 ing enzyme, PIPKIgammai2, functions with the proto-oncogene Src, to regulate oncogenic signaling.
259 eport that the RNA-binding protein (RBP) and proto-oncogene SRSF1 (serine and arginine-rich splicing
260 a hallmark of KS by unique activation of the proto-oncogene STAT3, coupled with MK2-mediated inactiva
261 errantly expressed both stem cell-associated proto-oncogenes, such as Lmo2, Hhex, Lyl1, and Kit, whic
265 53 with a gain of function (GOF), creating a proto-oncogene that contributes to tumorigenesis, tumor
268 ge of Mer tyrosine receptor kinase (MerTK, a proto-oncogene that plays a critical role in phagocytosi
269 oinositide 3-kinase enhancer A (PIKE-A) is a proto-oncogene that promotes tumor growth and transforma
270 as-like DNA in the 5'-UTR and 3'-UTR of four proto-oncogenes that are up-regulated in their transcrip
271 ascribed to PDAC with mutations in the KRAS2 proto-oncogene thought to be an early event in the progr
272 ed in hepatocellular carcinoma and acts as a proto-oncogene through Wnt pathway activation and induct
274 e is known about how the transformation from proto-oncogene to activated oncogene drives the expressi
275 f escape whereby tumor cells upregulated the proto-oncogene transcriptional regulators c-MYC and YAP1
277 d a novel oncogenic fusion involving the MER proto-oncogene tyrosine kinase (MERTK) and discovered a
279 hagocytosis due to a deficiency of the c-Mer proto-oncogene tyrosine kinase (Mertk) nonetheless conta
280 We now show that signaling through the Mer proto-oncogene tyrosine kinase (MerTK) receptor in cultu
282 eptor antagonists atrasentan and zibotentan, proto-oncogene tyrosine-protein kinase (SRC) inhibitor d
284 (miR200c, miR20b, and miR31through cellular proto-oncogene tyrosine-protein kinase Src (cSrc)), resp
285 phorylated by the tyrosine kinases p60c-Src (proto-oncogene tyrosine-protein kinase) and the proline-
286 ng that the HER2 oncogene, as opposed to the proto-oncogene, upregulates expression of the E2F2 trans
288 in leukemogenesis by causing deregulation of proto-oncogenes via relocation of cryptic regulatory DNA
293 hat it is cleaved and interacts with the JUN proto-oncogene, which forms part of the activator protei
295 emonstrate that overexpression of eIF4E, the proto-oncogene whose activity is specifically inhibited
296 These results suggest that MAGE-A11 is a proto-oncogene whose increased expression in prostate ca
297 ous studies have demonstrated that CREB is a proto-oncogene whose overexpression promotes cellular pr
298 rentiation, and were established early on as proto-oncogenes, with aberrant expression linked to tumo
299 r matrix and elevated expression of specific proto-oncogenes within the adjacent epithelium represent
300 evious results, we hypothesized that the MYC proto-oncogene would show differential expression in pRC
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