ライフサイエンスコーパス: v-Myb

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 SOD5 encodes a v-myb avian myeloblastosis viral oncogene homolog (MYB)

25 ly of salivary gland origin, has a signature v-myb avian myeloblastosis viral oncogene homolog-nuclea

26 P and v-Myb bind different DNA sequences in vitro.

27 t repressor of transcriptional activation by v-Myb but not c-Myb.

28 vely studied as a transcriptional activator, v-Myb can repress biologically relevant genes such as Et

29 f the N and/or C terminus of c-Myb, found in v-Myb, can potentiate its transforming ability.

30 The v-Myb conformation is thus suggested to play a critical

31 arboxyl terminus of c-Myb that is deleted in v-Myb contains negative regulatory domains.

32 The v-Myb DNA-binding domain differs from that of c-Myb main

33 bit transcription when activated through the v-Myb DNA-binding domain, but not the c-Myb DNA-binding

34 and CCd, while doubly truncated Myb proteins v-Myb (dVd) and dCd did not exhibit any differences in t

35 The nuclear protein v-Myb, encoded by the avian myeloblastosis virus (AMV),

36 hown that some genes that are regulated by a v-Myb-ER fusion protein may not be relevant to the biolo

37 Nevertheless, transformation by a v-Myb-ER fusion was estrogen dependent, and upon withdra

38 The Ets-2 gene was not expressed in v-Myb-ER transformed cells in the presence of estradiol,

39 presence but not the absence of estradiol in v-Myb-ER transformed cells.

40 LIM-3 expression was estradiol-inducible in v-Myb-ER transformed monoblasts, LIM-3 was expressed nei

41 cells transformed by a retrovirus encoding a v-Myb-estrogen receptor (ER) fusion protein.

42 Each type of mutation that distinguished v-Myb from c-Myb, including the N- and C-terminal deleti

43 Both c-Myb and v-Myb functioned as repressors and reduce the basal acti

44 The N terminus of v-Myb functions as the DNA-binding domain, and multiple

45 peat region of c-Myb that is also present in v-Myb functions only in conjunction with the Myb DNA-bin

46 The avian retroviral v-myb gene and its cellular homologues throughout the an

47 Thus, the v-myb gene encoded by the Avian Myeloblastosis Virus, is

48 We conclude that although v-Myb has been intensively studied as a transcriptional

49 hout affecting transcriptional activation by v-Myb in budding yeast.

50 The results suggest that v-Myb is not just a de-repressed version of c-Myb.

51 T cell lymphomas develop, demonstrating that v-Myb is oncogenic in T cells.

52 To date, v-myb is the only myb gene directly implicated in tumori

53 t studies have demonstrated that A-myb, like v-myb, is a potent transcriptional activator, raising th

54 factor, in cooperation with either c-Myb or v-Myb, is active in the combinatorial activation of myel

55 d by all of the mutants analyzed here except v-Myb itself exhibited the same phenotype as those trans

56 ement of the c-myb proto-oncogene to yield a v-Myb-like protein leads to myeloid and B cell lymphomas

57 V-myb myeloblastosis viral oncogene homolog (MYB) protei

58 rimary yolk sac cells transformed by unfused v-Myb nor in BM2 cells.

59 To study the effects of deregulation of v-Myb on T cell development, we have generated lines of

60 The v-Myb oncogene causes late onset T cell lymphomas when e

61 The v-Myb oncogene causes monoblastic leukemia and transform

62 The v-myb oncogene of the avian myeloblastosis virus (AMV) i

63 The v-myb oncogene of the avian myeloblastosis virus has led

64 In order to make conditional alleles of the v-myb oncogene, we constructed and tested avian retrovir

65 uctural and functional similarities with the v-myb oncogene.

66 The v-Myb oncoprotein encoded by Avian Myeloblastosis Virus

67 erated lines of transgenic mice in which the v-Myb oncoprotein is expressed in a T-cell-specific fash

68 nimal transcription activation domain of the v-Myb oncoprotein was initially mapped to a central clus

69 tive regulatory domain that is absent in the v-Myb oncoprotein, but conserved among all the known Myb

70 the AML1-ETO, AML1-MDS1, CBFbeta-SMMHC, and v-Myb oncoproteins.

71 In contrast, the full length v-Myb protein from BM2 cells only bound to the middle on

72 The v-Myb protein is a mutated and truncated version of c-My

73 The v-Myb protein is nuclear and binds to specific DNA seque

74 n electrophoretic mobility shift assays, the v-Myb protein is shown to be present in different confor

75 nt to the biological function of the unfused v-Myb protein.

76 The c-Myb and v-Myb proteins are transcription factors that regulate c

77 hat is recognized by an antibody against the v-myb repeat domain.

78 v-Myb, the transforming protein of avian myeloblastosis

79 w analyzed a series of C-terminal mutants of v-Myb to further investigate this domain.

80 phorbol ester-induced differentiation of the v-Myb-transformed BM2 cell line.

81 Analysis of T cell development in the v-Myb transgenic mice shows that ectopic expression of v

82 h s-Myb to cause lymphomas, we have infected v-Myb transgenic mice with Moloney murine leukemia virus

83 To identify genes regulated by v-Myb, we utilized primary cells transformed by a retrov

84 chanism underlying the oncogenic activity of v-Myb, which appears to be a stronger transcriptional ac

85 to bind or inhibit the oncogenic derivative v-Myb, which has a mutated Cyp-40 binding site.

86 his region is essential for the functions of v-Myb without requiring a heptad leucine repeat.