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1 itially called mab or amv, but later renamed v-myb).
2 ted to the different activities of c-Myb and v-Myb.
3  for increasing the transforming activity of v-Myb.
4 as created by combining Myb repeats of P and v-Myb.
5  distinct DNA binding specificities of P and v-Myb.
6 intaining a fully functional conformation of v-Myb.
7 to play a critical role in the regulation of v-Myb activity.
8 sgenic mice shows that ectopic expression of v-Myb affects the ratio of helper to cytotoxic T cells,
9      These results suggest that mutations in v-Myb allow it to evade a negative regulatory mechanism
10 l activation and oncogenic transformation by v-Myb Amv.
11                                   Therefore, v-myb and c-myb can cooperate to induce T cell lymphomas
12 ific genomic rearrangement between potential v-myb and c-myb consensus binding sites within introns 2
13 his differential effect of D-type cyclins on v-Myb and c-Myb might help to explain the mechanism unde
14                          In human cells, the v-Myb and c-Myb proteins displayed strikingly different
15 e combined structure-function studies of the v-Myb and c-Myb proteins with unbiased microarray-based
16                  Our results show that while v-myb and c-myb transactivated transcription equally wel
17    Differences in the DNA binding domains of v-Myb and P, which are conserved among animal and plant
18  number of different fusion proteins between v-Myb and the human estrogen receptor (ER).
19      Furthermore, IFN regulatory factor 1, c/v-Myb, and p53 binding sites are present in the promoter
20                  This exon is not present in v-myb, and proteins containing these amino acids have ne
21 l3 which harbor myb transgenes; derived from v-myb, and the ABPL-1, ABPL-2, ABPL-4 and NFS-60 cell li
22      Regions flanking this central domain of v-Myb are required for transcriptional activation by the
23 two angiocentric gliomas in the related gene v-myb avian myeloblastosis viral oncogene homolog (MYB)
24 ly of salivary gland origin, has a signature v-myb avian myeloblastosis viral oncogene homolog-nuclea
25                                        P and v-Myb bind different DNA sequences in vitro.
26 t repressor of transcriptional activation by v-Myb but not c-Myb.
27 vely studied as a transcriptional activator, v-Myb can repress biologically relevant genes such as Et
28 f the N and/or C terminus of c-Myb, found in v-Myb, can potentiate its transforming ability.
29                                          The v-Myb conformation is thus suggested to play a critical
30 arboxyl terminus of c-Myb that is deleted in v-Myb contains negative regulatory domains.
31                                          The v-Myb DNA-binding domain differs from that of c-Myb main
32 bit transcription when activated through the v-Myb DNA-binding domain, but not the c-Myb DNA-binding
33 and CCd, while doubly truncated Myb proteins v-Myb (dVd) and dCd did not exhibit any differences in t
34                          The nuclear protein v-Myb, encoded by the avian myeloblastosis virus (AMV),
35 hown that some genes that are regulated by a v-Myb-ER fusion protein may not be relevant to the biolo
36            Nevertheless, transformation by a v-Myb-ER fusion was estrogen dependent, and upon withdra
37          The Ets-2 gene was not expressed in v-Myb-ER transformed cells in the presence of estradiol,
38 presence but not the absence of estradiol in v-Myb-ER transformed cells.
39  LIM-3 expression was estradiol-inducible in v-Myb-ER transformed monoblasts, LIM-3 was expressed nei
40 cells transformed by a retrovirus encoding a v-Myb-estrogen receptor (ER) fusion protein.
41     Each type of mutation that distinguished v-Myb from c-Myb, including the N- and C-terminal deleti
42                               Both c-Myb and v-Myb functioned as repressors and reduce the basal acti
43                            The N terminus of v-Myb functions as the DNA-binding domain, and multiple
44 peat region of c-Myb that is also present in v-Myb functions only in conjunction with the Myb DNA-bin
45                         The avian retroviral v-myb gene and its cellular homologues throughout the an
46                                    Thus, the v-myb gene encoded by the Avian Myeloblastosis Virus, is
47                    We conclude that although v-Myb has been intensively studied as a transcriptional
48 hout affecting transcriptional activation by v-Myb in budding yeast.
49                     The results suggest that v-Myb is not just a de-repressed version of c-Myb.
50 T cell lymphomas develop, demonstrating that v-Myb is oncogenic in T cells.
51                                     To date, v-myb is the only myb gene directly implicated in tumori
52 t studies have demonstrated that A-myb, like v-myb, is a potent transcriptional activator, raising th
53  factor, in cooperation with either c-Myb or v-Myb, is active in the combinatorial activation of myel
54 d by all of the mutants analyzed here except v-Myb itself exhibited the same phenotype as those trans
55 ement of the c-myb proto-oncogene to yield a v-Myb-like protein leads to myeloid and B cell lymphomas
56                                              V-myb myeloblastosis viral oncogene homolog (MYB) protei
57 rimary yolk sac cells transformed by unfused v-Myb nor in BM2 cells.
58      To study the effects of deregulation of v-Myb on T cell development, we have generated lines of
59                                          The v-Myb oncogene causes late onset T cell lymphomas when e
60                                          The v-Myb oncogene causes monoblastic leukemia and transform
61                                          The v-myb oncogene of the avian myeloblastosis virus (AMV) i
62                                          The v-myb oncogene of the avian myeloblastosis virus has led
63  In order to make conditional alleles of the v-myb oncogene, we constructed and tested avian retrovir
64 uctural and functional similarities with the v-myb oncogene.
65                                          The v-Myb oncoprotein encoded by Avian Myeloblastosis Virus
66 erated lines of transgenic mice in which the v-Myb oncoprotein is expressed in a T-cell-specific fash
67 nimal transcription activation domain of the v-Myb oncoprotein was initially mapped to a central clus
68 tive regulatory domain that is absent in the v-Myb oncoprotein, but conserved among all the known Myb
69  the AML1-ETO, AML1-MDS1, CBFbeta-SMMHC, and v-Myb oncoproteins.
70                 In contrast, the full length v-Myb protein from BM2 cells only bound to the middle on
71                                          The v-Myb protein is a mutated and truncated version of c-My
72                                          The v-Myb protein is nuclear and binds to specific DNA seque
73 n electrophoretic mobility shift assays, the v-Myb protein is shown to be present in different confor
74 nt to the biological function of the unfused v-Myb protein.
75                                The c-Myb and v-Myb proteins are transcription factors that regulate c
76 hat is recognized by an antibody against the v-myb repeat domain.
77                                              v-Myb, the transforming protein of avian myeloblastosis
78 w analyzed a series of C-terminal mutants of v-Myb to further investigate this domain.
79 phorbol ester-induced differentiation of the v-Myb-transformed BM2 cell line.
80        Analysis of T cell development in the v-Myb transgenic mice shows that ectopic expression of v
81 h s-Myb to cause lymphomas, we have infected v-Myb transgenic mice with Moloney murine leukemia virus
82               To identify genes regulated by v-Myb, we utilized primary cells transformed by a retrov
83 chanism underlying the oncogenic activity of v-Myb, which appears to be a stronger transcriptional ac
84  to bind or inhibit the oncogenic derivative v-Myb, which has a mutated Cyp-40 binding site.
85 his region is essential for the functions of v-Myb without requiring a heptad leucine repeat.

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