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1 ene homolog (Kras), or overexpression of MYC proto-oncogene.
2 h splicing factor 3 (SRSF3 or SRp20) being a proto-oncogene.
3 gulation, like P53 tumor suppressor and cMYC proto-oncogene.
4 GCM2, suggesting that GCM2 is a parathyroid proto-oncogene.
5 in the rearranged during transfection (RET) proto-oncogene.
6 ative transcription factor may also act as a proto-oncogene.
7 emia through aberrant expression of the EVI1 proto-oncogene.
8 F2alpha regulation is JNK dependent, via jun proto-oncogene.
9 lowing for quantitative analysis of the cMYC proto-oncogene.
10 inhibitors, and overexpression of the c-Myc proto-oncogene.
11 the estrogen receptor coregulator PELP1 is a proto-oncogene.
12 has previously been described as a powerful proto-oncogene.
13 r and therefore generally considered to be a proto-oncogene.
14 t into the categorization of ECT2 as a human proto-oncogene.
15 ss mRNAs including the mRNA encoding the Mos proto-oncogene.
16 driven by an activating mutation in the KIT proto-oncogene.
17 c prostate cancer cells is driven by the MYC proto-oncogene.
18 nent for understanding the role of AGR2 as a proto-oncogene.
19 onmalignant cells was sufficient to activate proto-oncogenes.
20 ted neighborhoods containing prominent T-ALL proto-oncogenes.
21 druplex structures are found in promoters of proto-oncogenes.
22 ain of specific genomic loci known to harbor proto-oncogenes.
23 activate tumor suppressor genes and activate proto-oncogenes.
24 factor activity of the NOTCH1, MYC, and IRF4 proto-oncogenes.
25 ques that regulate the expression of crucial proto-oncogenes.
27 is regulated by the transcription factor ETS proto-oncogene 1 (ETS1) and associated with overexpressi
28 e closely linked E26 transformation-specific proto-oncogene 1 (ETS1) is overexpressed in these FLI1-d
29 inases anaplastic lymphoma kinase (ALK), ROS proto-oncogene 1 (ROS1) and rearranged during transfecti
30 stic lymphoma kinase (ALK)-rearranged or ROS proto-oncogene 1 (ROS1)-rearranged non-small-cell lung c
31 h pathways dependent or not dependent on ABL proto-oncogene 1 non-receptor tyrosine kinase (c-Abl).
32 ncided with a 4.5-fold increase in ETS1 (ETS proto-oncogene 1) mRNA, suggesting that ETS1 is involved
34 9 resides within the SH3-binding site of ABL proto-oncogene 1, nonreceptor tyrosine kinase (ABL1), so
35 tibody and a breakpoint cluster region - ABL proto-oncogene 1, nonreceptor tyrosine kinase (BCR-ABL1)
37 en GTPase, as small GTPases such as RAS-like proto-oncogene A (RALA) or the G12C mutant of KRAS displ
41 gammaretrovirus vectors have caused cellular proto-oncogene activation and leukemia, necessitating th
42 om an index patient and demonstrate that MET proto-oncogene activation is important for tumor growth
45 tidyl inositol 3 kinase (PI3K)-thymoma viral proto-oncogene (AKT) inhibitors to kill tumor cells.
46 regulated kinase (ERK) and the thymoma viral proto-oncogene (Akt), followed by activation of the mamm
47 indings establish roles for PLK1 as a potent proto-oncogene and a CIN gene and provide insights for t
49 are cell cycle regulators and function as a proto-oncogene and a tumor suppressor respectively in hu
51 and activates an LCR that regulates the BCL6 proto-oncogene and is uniquely required by normal and ma
52 ensin 1-7 and alamandine, which activate MAS proto-oncogene and MAS-related D receptors, respectively
53 esults therefore identify miR-22 as a potent proto-oncogene and suggest that aberrations in the miR-2
54 is study shows that Erk1 can be considered a proto-oncogene and that Erk molecules possess unusual au
55 ed by numerous common integration sites near proto-oncogenes and by increased abundance of clones wit
56 scription factor genes, including MYC family proto-oncogenes and neuroendocrine lineage-specific fact
57 e p53 mutations or undergo amplifications of proto-oncogenes and receptor tyrosine kinases, implicati
58 n-protein interactions, including binding to proto-oncogenes and tumor suppressors to regulate cell d
61 mily 2/3 (SMAD2/3)-dependent manner, and Jun proto-oncogene AP-1 transcription factor subunit (AP-1)
62 r the translation of the mRNAs of JUND (JunD proto-oncogene AP-1 transcription factor subunit) and HI
63 nctions, at least in part, by binding to Jun proto-oncogene, AP-1 transcription factor subunit (cJUN)
64 tor of activated T cells 3 (NFATc3) and FosB proto-oncogene, AP-1 transcription factor subunit (FosB)
66 to constitutive activation of NRAS and KRAS proto-oncogenes are among the most common in human cance
68 mation and autoimmunity identified the c-Fos proto-oncogene as a mediator of ER stress responses in e
71 nstream of KRAS, depletion of RalB (RAS-like proto-oncogene B) and IkappaB kinase-related TANK-bindin
73 he best-characterized PP2A substrates is MYC proto-oncogene basic helix-loop-helix transcription fact
74 man primary lymphocytes, and identificed the proto-oncogene BCL2 as a replication stress-induced frag
75 directly activated the transcription of the proto-oncogene BCL6 in normal germinal-center (GC) B cel
76 isms that prevent proteasomal degradation of proto-oncogene beta-catenin (CTNNB1) and its eventual tr
80 ing pathway, directed by the oncogenic B-Raf proto-oncogene (BRAF) variant BRAF(V600E), that mediates
82 y displays mutational activation of the KRAS proto-oncogene but, unlike lung cancers expressing mutat
83 t and PH domain 2) isoform 2 is considered a proto-oncogene, but not much is known about AGAP2 gene e
84 shown to be negatively modulated by the MYCN proto-oncogene, but the mechanism of repression was uncl
85 rticular, epigenetic derepression of the RET proto-oncogene by loss of PRC2 recruitment, and activati
86 , activation of otherwise normally repressed proto-oncogenes by promoter demethylation has been infre
87 d ATM-dependent signalling, and identify the proto-oncogene c-Abl as a mediator of this modification.
88 ssays, accompanied by enhanced expression of proto-oncogene C-Fms (C-Fms) and hyper-responsiveness to
89 y and FRET analyses, we demonstrate that the proto-oncogene c-Fos (c-Fos) activates cytoplasmic lipid
90 e shown that co-expression of TAp73 with the proto-oncogene c-Jun can augment cellular growth and pot
91 rrelation between GAPDH upregulation and the proto-oncogene c-jun expression (r = 0.543, P = .003).
93 ain-containing protein, SAMD14, promotes SCF/proto-oncogene c-Kit (c-Kit) signaling, erythroid progen
95 epidermal growth factor receptor (EGFR) and proto-oncogene c-Met (MET), and shunts their trafficking
96 ivity requires binding to its receptors, the proto-oncogene c-Met and heparan sulfate proteoglycan (H
97 oticed transcriptional repression of 5-LO by proto-oncogene c-Myb and conclude that loss of stromal 5
99 blocked at the polymorphic site and that the proto-oncogene c-MYB modulates the release of the pausin
101 reconstructed in cell culture, and that the proto-oncogene c-Myc controls the generation of self-ren
102 chromosome 8q24.21 locus, which contains the proto-oncogene c-MYC, long non-coding RNA PVT1, and micr
105 HPK1 increased the binding of AXL to the Cbl proto-oncogene (c-Cbl); promoted AXL ubiquitination; dec
106 MR) status and somatic mutation in the B-Raf proto-oncogene (c.1799T>A [V600E]; BRAFV600E) or exon 2
110 udies uncover a fine-tuned modulation of the proto-oncogene CCND1 in Ewing sarcoma cells via alternat
111 rp12(-/-) tumors showed higher expression of proto-oncogenes cJun and cMyc and downregulation of tumo
113 ied novel direct targets, including CRK-like proto-oncogene (CRKL) and focal adhesion kinase (FAK).
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
118 The RET (rearranged during transfection) proto-oncogene encodes a receptor tyrosine kinase for me
121 showed that miR-155 is coexpressed with the proto-oncogene encoding c-MYC in positively selected B c
123 ified genes shared by the two cell types are proto-oncogenes ERK2, a component of the ERK/MAPK pathwa
125 human androgen receptor (AR) coactivator and proto-oncogene expressed at low levels in normal human r
127 splayed intense tyrosine hydroxylase and RET proto-oncogene expression in nigral neurons in the patie
128 this method by examining copy number in the proto-oncogene FLT3 and the common V600E point mutation
129 e resulted in an increased expression of the proto-oncogenes FOS and JUN in both cell lines at 72 hr.
130 rough a series of studies, we identified the proto-oncogene fosab (cfos) as a potent miR-101a target
136 s potently drive human cancers, with mutated proto-oncogene GTPase KRAS4B (K-Ras4B) being the most ab
139 e discovery of potent inhibitors of the BRAF proto-oncogene has revolutionized therapy for melanoma h
140 binger DNA transposons carrying the Myb-like proto-oncogene have expanded dramatically in the Pleurod
142 nvadopodia component Tks5long, the embryonal proto-oncogene Hmga2, and the epithelial-to-mesenchymal
144 nslation of the mixed lineage leukemia (MLL) proto-oncogene in an arginine methylation-dependent mann
145 eased copy number and expression of the PIM1 proto-oncogene in genomic data sets of patients with TNB
147 a mechanism by which lncRNA MALAT1 acts as a proto-oncogene in hepatocellular carcinoma, modulating o
150 w mechanistic insights into the role of this proto-oncogene in stem cell differentiation, neuronal ag
151 Amplifications and mutations in the KIT proto-oncogene in subsets of melanomas provide therapeut
160 r BRCA1-deficient MBC by introducing the MET proto-oncogene into a BRCA1-associated breast cancer mod
161 expression strongly correlates with c-jun, a proto-oncogene involved in liver tumorigenesis in human
164 Expression of the MECOM (also known as EVI1) proto-oncogene is deregulated by chromosomal translocati
166 mplification and overexpression of erbB2/neu proto-oncogene is observed in 20-30% human breast cancer
168 30 (involved in membrane transport), and the proto-oncogene JUN, indicate that the Rab1b increase act
169 e transcription factor c-Jun, product of the proto-oncogene JUN, is a key regulator of mitochondrial
170 ents FBJ osteosarcoma oncogene (FOS) and jun proto-oncogene (JUN) to the promoters of a subset of Tol
171 regulation by retinoid X receptor (RXR), jun proto-oncogene (JUN), sine oculis homeobox factor (SIX),
172 onstrate the direct allosteric activation of proto-oncogene kinase Src by GPCR-betaarr complexes in v
177 >A [V600E]; BRAFV600E) or exon 2 of the KRAS proto-oncogene (KRAS) in the primary tumor with SAR in p
179 mutations in the RET (formerly MEN2A, MEN2B) proto-oncogene located on chromosomal band 10q11.21.
181 type 2 angiotensin II receptor (AT(2)R), the proto-oncogene Mas receptor and the Mas-related G protei
183 xemplified by antibodies, an E3 ligase, MDM2 proto-oncogene (MDM2), and protease (SplB from Staphyloc
185 signaling uses lateral activation of the met proto-oncogene (MET) through SRC proto-oncogene nonrecep
188 These include the signaling gene TGFBR1, the proto-oncogene MYB as well as many immune-related genes
190 strong, haplotype-specific activation of the proto-oncogene MYC by the integrated HPV-18 genome appro
193 vates myofibroblast cell identity genes, the proto-oncogene Myc, and an array of genes encoding pro-i
194 lso been implicated in the repression of the proto-oncogene Myc, but the mechanism has remained uncle
196 We investigated the activities of the RELB proto-oncogene NF-kappaB subunit in human cholangiocytes
197 ated ITG-dependent focal adhesion kinase/Src proto-oncogene non-receptor tyrosine kinase signaling.
199 of the met proto-oncogene (MET) through SRC proto-oncogene nonreceptor tyrosine kinase to maximize c
201 domain and is directly phosphorylated by SRC proto-oncogene, nonreceptor tyrosine kinase (SRC) at Tyr
203 ing of late endosomes allows delivery of SRC proto-oncogene, nonreceptor tyrosine kinase (SRC) to the
206 lated neighborhoods, we investigated whether proto-oncogenes occur within these structures and whethe
209 en initiated by genetic events that activate proto-oncogenes or inactivate tumor-suppressor genes.
210 Here, we identify the protein kinase and proto-oncogene PIM3 as being repressed downstream of mTO
211 ayed highly significant up-regulation of the proto-oncogene pleomorphic adenoma gene 1 (PLAG1), sugge
212 tes expression of CDKN2a/p16(INK4a) and BMI1 proto-oncogene polycomb ring finger (BMI1), with the lat
213 ver, whether the human mTOR gene itself is a proto-oncogene possessing tumorigenicity has not been fi
215 subunits and "small" G proteins, such as the proto-oncogene product RAS, which contains a single subu
216 SF) and its receptor, the product of the MET proto-oncogene, promote invasion and metastasis of tumor
217 pe was observed by overexpressing c-Myc (Myc proto-oncogene protein), a downstream target of Pim kina
218 ine phosphatase (PTP) SHP2 is encoded by the proto-oncogene PTPN11 and is a ubiquitously expressed ke
220 el in Drosophila, oncogenic mutations of the proto-oncogene Ras (Ras(V12)) maintain tumorous cells in
221 tiated hepatocyte growth factor (HGF) to MET proto-oncogene receptor tyrosine kinase (c-Met) autocrin
222 nfluences the prognostic significance of KIT proto-oncogene receptor tyrosine kinase (KIT) and platel
223 aberrant hepatocyte growth factor (HGF)/MET proto-oncogene receptor tyrosine kinase (MET) and Wnt/be
224 , we report that signalling engaging the MET proto-oncogene receptor tyrosine kinase/focal adhesion k
225 Resistance to approved inhibitors of KIT proto-oncogene, receptor tyrosine kinase (KIT), and plat
226 GDNF family receptor alpha like (GFRAL)-Ret proto-oncogene (RET) signaling complex in brainstem neur
228 ned for an alternatively spliced exon in the proto-oncogene RON and determine the functional units th
230 ncreased interaction of the RAS ITD with Raf proto-oncogene Ser/Thr kinase (RAF), leading to increase
231 roscopy, we demonstrated that KRAS and Raf-1 proto-oncogene Ser/Thr kinase (RAF1) domains interact wi
232 the presence of inhibitors targeting the RAF proto-oncogene Ser/Thr protein kinase (RAF) and MAPK/ERK
236 r of cytokine signaling 2/3 (Socs2/3); Pim-1 proto-oncogene, Ser/Thr kinase (Pim1); and Fms-related t
237 endent release of insulin, activation of RAF proto-oncogene, Ser/Thr kinase (Raf)-mitogen-activated p
238 the identification of clients, such as Raf-1 proto-oncogene, Ser/Thr kinase (RAF1), that are particul
241 pG island methylator phenotype (CIMP), B-Raf proto-oncogene serine/threonine kinase (BRAF) mutation,
242 ard, which in turn gradually suppressed RAF1 proto-oncogene serine/threonine kinase (RAF1)/ERK signal
243 Here, we report the efficacy of the Raf proto-oncogene serine/threonine protein kinase (RAF) inh
244 ted HRAS(G12V) with its effector protein RAF proto-oncogene serine/threonine protein kinase 1 (RAF1).
246 se methylesterase 1 (PME-1), and SET nuclear proto-oncogene (SET) that often are deregulated in cance
247 errant HGF-MET (hepatocyte growth factor-met proto-oncogene) signaling activation via interactions wi
248 variation in ten individuals with SGS in the proto-oncogene SKI, a known repressor of TGF-beta activi
249 bited antifibrotic Sloan-Kettering Institute proto-oncogene (Ski) and Ski-related novel gene, non-Alu
250 ical T-cell signaling pathway, including LCK proto-oncogene SRC family tyrosine kinase (LCK), LYN pro
251 cogene SRC family tyrosine kinase (LCK), LYN proto-oncogene SRC family tyrosine kinase (LYN), zeta ch
254 ing enzyme, PIPKIgammai2, functions with the proto-oncogene Src, to regulate oncogenic signaling.
258 eport that the RNA-binding protein (RBP) and proto-oncogene SRSF1 (serine and arginine-rich splicing
259 a hallmark of KS by unique activation of the proto-oncogene STAT3, coupled with MK2-mediated inactiva
261 ation of hepatocellular carcinoma-associated proto-oncogenes such as c-Jun and associated transcripti
263 errantly expressed both stem cell-associated proto-oncogenes, such as Lmo2, Hhex, Lyl1, and Kit, whic
266 53 with a gain of function (GOF), creating a proto-oncogene that contributes to tumorigenesis, tumor
269 ge of Mer tyrosine receptor kinase (MerTK, a proto-oncogene that plays a critical role in phagocytosi
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
275 f escape whereby tumor cells upregulated the proto-oncogene transcriptional regulators c-MYC and YAP1
276 e, to investigate the interplay between IGH@ proto-oncogene translocation and IGH allelic exclusion,
279 d a novel oncogenic fusion involving the MER proto-oncogene tyrosine kinase (MERTK) and discovered a
281 hagocytosis due to a deficiency of the c-Mer proto-oncogene tyrosine kinase (Mertk) nonetheless conta
282 We now show that signaling through the Mer proto-oncogene tyrosine kinase (MerTK) receptor in cultu
285 (miR200c, miR20b, and miR31through cellular proto-oncogene tyrosine-protein kinase Src (cSrc)), resp
286 ar alterations of YES1, a member of the SRC (proto-oncogene tyrosine-protein kinase Src) family kinas
287 ORC2 targets included focal adhesion kinase, proto-oncogene tyrosine-protein kinase Src, and caveolin
288 phorylated by the tyrosine kinases p60c-Src (proto-oncogene tyrosine-protein kinase) and the proline-
289 ng that the HER2 oncogene, as opposed to the proto-oncogene, upregulates expression of the E2F2 trans
291 in leukemogenesis by causing deregulation of proto-oncogenes via relocation of cryptic regulatory DNA
296 hat it is cleaved and interacts with the JUN proto-oncogene, which forms part of the activator protei
297 emonstrate that overexpression of eIF4E, the proto-oncogene whose activity is specifically inhibited
298 These results suggest that MAGE-A11 is a proto-oncogene whose increased expression in prostate ca
299 rentiation, and were established early on as proto-oncogenes, with aberrant expression linked to tumo
300 evious results, we hypothesized that the MYC proto-oncogene would show differential expression in pRC