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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.
8 sgenic mice shows that ectopic expression of v-Myb affects the ratio of helper to cytotoxic T cells,
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
15 e combined structure-function studies of the v-Myb and c-Myb proteins with unbiased microarray-based
17 Differences in the DNA binding domains of v-Myb and P, which are conserved among animal and plant
21 l3 which harbor myb transgenes; derived from v-myb, and the ABPL-1, ABPL-2, ABPL-4 and NFS-60 cell li
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
27 vely studied as a transcriptional activator, v-Myb can repress biologically relevant genes such as Et
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
35 hown that some genes that are regulated by a v-Myb-ER fusion protein may not be relevant to the biolo
39 LIM-3 expression was estradiol-inducible in v-Myb-ER transformed monoblasts, LIM-3 was expressed nei
41 Each type of mutation that distinguished v-Myb from c-Myb, including the N- and C-terminal deleti
44 peat region of c-Myb that is also present in v-Myb functions only in conjunction with the Myb DNA-bin
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
63 In order to make conditional alleles of the v-myb oncogene, we constructed and tested avian retrovir
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
73 n electrophoretic mobility shift assays, the v-Myb protein is shown to be present in different confor
81 h s-Myb to cause lymphomas, we have infected v-Myb transgenic mice with Moloney murine leukemia virus
83 chanism underlying the oncogenic activity of v-Myb, which appears to be a stronger transcriptional ac
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