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1 ivated the MEK/ERK pathway as efficiently as v-Raf.
2 Ha-rasV12, which in turn was greater than by v-raf.
3 oblasts by v-crk, -src, and -ras, but not by v-raf.
4  block transformation mediated by v-H-Ras or v-Raf.
5 ed phosphorylation of protein kinase Balpha, v-raf-1 murine leukemia viral oncogene homolog 1 (i.e.,
6                                              V-raf-1 murine leukemia viral oncogene homolog 1 (Raf-1)
7 pathway, comprising the protein kinases RAF (v-raf-1 murine leukemia viral oncogene homolog 1), MEK1/
8 an cancers, due to mutations in RAS or BRAF (v-raf-1 murine leukemia viral oncogene homolog B1).
9 F1 (epithelial splicing regulatory protein-1-v-raf-1 murine leukemia viral oncogene homolog-1) gene f
10 f RhoA is required for efficient (V12)HaRas, V-Raf and (V600E)BRAF transformation and (V12)HaRas-medi
11 n, we treated rat 3Y1 fibroblasts expressing v-Raf and showed that the antibiotic blocked assembly of
12 by cotransfection with constitutively active v-raf and was blocked by the dominant-negative mutant, c
13 rea was increased by srcF527, Ha-rasV12, and v-raf, and although it altered myocyte morphology by cau
14             Various oncogenes such as c-Src, v-Raf, and Ras, and multiple environmental stimuli, incl
15  in REF-1 cells transformed by v-ras, v-src, v-raf, and v-fos.
16 nts to estradiol or stable expression of the v-raf construct yielded cells that extended processes at
17 but only in combination can they translocate v-Raf (delta gag) into the nucleolus.
18 is sufficient to translocate the cytoplasmic v-Raf (delta gag) into the nucleus, but only in combinat
19 authentic NoLS, BR2 was fused to cytoplasmic v-Raf (delta gag) kinase.
20     Several protein kinases (e.g. pp60(src), v-Raf) exist in heterocomplexes with hsp90 and a 50-kDa
21 ated kinase cascade (srcF527, Ha-rasV12, and v-raf) increased expression of "fetal" genes.
22 educed dramatically (6-8-fold) the number of v-raf-induced foci in transfected NIH3T3 cells.
23 oncogenic protein kinases, such as v-Src and v-Raf, into heterocomplexes that contain hsp90 and eithe
24 rising from the V600E mutation in the kinase v-RAF murine sarcoma viral oncogene homolog B (BRAF(V600
25                                              v-raf murine sarcoma viral oncogene homolog B (BRAF) and
26 e NPs efficiently silences the expression of V-Raf murine sarcoma viral oncogene homolog B (BRAF) in
27 hatase, receptor type, O cooperated with the v-raf murine sarcoma viral oncogene homolog B (BRAF) rec
28                 Frequent somatic mutation of v-raf murine sarcoma viral oncogene homolog B (BRAF), a
29 ng rearranged during transfection (RET)/PTC, v-RAF murine sarcoma viral oncogene homolog B (BRAF), or
30                                        BRAF (v-raf murine sarcoma viral oncogene homolog B) inhibitor
31              Melanoma cells driven by mutant v-raf murine sarcoma viral oncogene homolog B1 (B-RAF) a
32 reviously identified activating mutations of v-raf murine sarcoma viral oncogene homolog B1 (BRAF) (B
33 requently driven by mutational activation of v-raf murine sarcoma viral oncogene homolog B1 (BRAF) ac
34               Although melanomas with mutant v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) ca
35 at melanomas and to increase the duration of v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) in
36 hibitor as single therapy or together with a v-raf murine sarcoma viral oncogene homolog B1 (BRAF) in
37 fenib and dabrafenib selectively inhibit the v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) ki
38         We have shown previously that mutant v-raf murine sarcoma viral oncogene homolog B1 (BRAF) me
39 henotype (CIMP), microsatellite instability, v-raf murine sarcoma viral oncogene homolog B1 (BRAF) mu
40  issue of Blood, Xi and colleagues report on v-raf murine sarcoma viral oncogene homolog B1 (BRAF) mu
41 discovery of cross-talk between the AMPK and v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) si
42 ted protein kinase signaling pathway such as v-raf murine sarcoma viral oncogene homolog B1 (BRAF), v
43 l transduction molecule has been identified: v-raf murine sarcoma viral oncogene homolog B1 (BRAF).
44 r (VEGF), rearranged during transfection and v-raf murine sarcoma viral oncogene homolog B1 pathways
45 5A3-BRAF (solute carrier family 45, member 3-v-raf murine sarcoma viral oncogene homolog B1) and ESRP
46 To evaluate the timing of mutations in BRAF (v-raf murine sarcoma viral oncogene homolog B1) during m
47 and mutations sought in exon 15 of the BRAF (v-raf murine sarcoma viral oncogene homolog B1) gene usi
48 odine (RAI), have a high prevalence of BRAF (v-raf murine sarcoma viral oncogene homolog B1) mutation
49  harboring activating mutations in the BRAF (V-raf murine sarcoma viral oncogene homolog B1) oncogene
50 ptimization of a series of new inhibitors of V-RAF murine sarcoma viral oncogene homologue B1 (BRAF),
51 eceptor 2, anaplastic lymphoma kinase (ALK), v-Raf murine sarcoma viral oncogene homologue B1, AKT, B
52 over, we show that, like Mos, both v-ras and v-raf oncogene products induce apoptosis in p53+/+ MEFs.
53 , nor could previous transformation with the v-raf oncogene.
54 resses the transforming activity of H-ras or v-raf oncogenes through ERK dephosphorylation and inacti
55 function of transformation by the Ha-ras and v-raf oncogenes, evaluations of the signaling and transc
56 ed morphological transformation by H-ras and v-raf oncogenes.
57 tion, we stably transfected H19-7 cells with v-raf or an oncogenic human Raf-1-estrogen receptor fusi
58                      However, in contrast to v-Raf, RafS259 mutants failed to transform.
59 tially discovered in the viral Raf oncogene (v-Raf), results in a kinase domain with high basal activ
60             To obtain some insight as to how v-Raf selects predominantly hsp90.p50(cdc37) heterocompl
61 d the vimentin phosphopeptides isolated from v-raf-transfected cells labeled with orthophosphoric aci
62 emonstrate an association between Ha-ras and v-raf transformation of CREF cells with elevated PEA3 an
63 ic transforming genes, like v-abl, v-ras, or v-raf, which did not confer indefinite division potentia
64 o, we show that p50(cdc37) binds directly to v-Raf, with the catalytic domain of Raf being sufficient

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