ライフサイエンスコーパス: abl oncogene

1 eloid precursor cells transformed by the BCR/ABL oncogene.

2 of a primitive hematopoietic cell by the BCR/ABL oncogene.

3 hways, including those downstream of the bcr-abl oncogene.

4 ion, NK92 cells were transduced with the BCR/ABL oncogene.

5 ial for the transforming activity of the Bcr/Abl oncogene.

6 acute transforming retrovirus encoding the v-abl oncogene.

7 ith wild-type versus mutant forms of the Bcr/Abl oncogene.

8 insic oncogenic properties of the particular abl oncogene.

9 c leukemia (B-ALL) and is induced by the BCR-ABL oncogene.

10 transformation of immature B cells by the v-abl oncogene.

11 eration, including transformation by the Bcr-Abl oncogene.

12 protein that is a major substrate of the BCR/ABL oncogene.

13 mechanisms in B-lineage cells transformed by ABL oncogenes.

14 I3K signaling in B-lineage transformation by ABL oncogenes.

15 ability of cells transformed by any of these ABL oncogenes.

16 C-abl oncogene 1, nonreceptor tyrosine kinase (ABL1) kinas

17 n of hematopoietic cells by the chimeric Bcr-Abl oncogene, a highly activated tyrosine kinase.

18 The v-Abl oncogene activates Jak-Stat signaling during transfo

19 dy the molecular mechanisms by which the bcr-abl oncogene acts in the disease progression of CML.

20 vo evidence for the proapoptotic function of Abl.Oncogene advance online publication, 18 December 200

21 dependent on continuous signaling of the BCR-ABL oncogene, also termed oncogene addiction, reprogramm

22 rate implicated in transformation by the bcr-abl oncogene and in signaling by cytokines.

23 and pre-B cells are the target cells of the abl oncogene and numerous studies have suggested that St

24 a-positive CML (Ph(+) CML) caused by the BCR-ABL oncogene, and in this condition, morgana underexpres

25 the Philadelphia (Ph) chromosome-encoded BCR-ABL oncogene, and these tend to have a poor prognosis.

26 Dami/HEL cells do not express the BCR/ABL oncogene, but increased constitutive phosphorylation

27 acutely transformed by the CML-specific BCR-ABL oncogene, but not by the serine kinase oncogene v-MO

28 lines K562 and BV173, which express the Bcr/Abl oncogene, but not in several Bcr/Abl-negative leukem

29 th a retrovirus vector carrying an activated ABL oncogene can be analysed.

30 Activated ABL oncogenes cause B-cell leukemias in mice and chronic

31 The BCR/ABL oncogene causes chronic myelogenous leukemia (CML),

32 The BCR/ABL oncogene causes chronic myelogenous leukemia, a myel

33 The BCR/ABL oncogene causes human chronic myelogenous leukemia (

34 oint cluster region-ABL tyrosine kinase (BCR-ABL) oncogene causes chronic myelogenous leukemia (CML).

35 These results suggest that the BCR/ABL oncogene could alter the function of p130(CAS) in at

36 Cellular transformation by the BCR/ABL oncogene depends on the ABL-encoded tyrosine kinase

37 olytic human immune response against CML bcr-abl oncogene-derived peptides and provide a rationale fo

38 STAT5 might be one part of the mechanism of abl oncogene disease specificity.

39 The BCR/ABL oncogene encodes an activated tyrosine kinase that c

40 The BCR-ABL oncogene encodes an in-frame fusion protein containi

41 the chronic myeloid leukemia-associated BCR/ABL oncogene endows the adult hematopoietic stem cell wi

42 lphia chromosome (Ph) translocation, the BCR/ABL oncogene, exists in three principal forms (P190, P21

43 Here we demonstrate that in the Bcr-abl oncogene expressing human leukemia K562 cells, HDAC6

44 hether the apparent specificity of these two abl oncogenes for myeloid versus lymphoid neoplasms is d

45 The Bcr-Abl oncogene, found in Philadelphia chromosome-positive

46 ifferentiation and the expression of the BCR-ABL oncogene has direct relevance to CML biology as well

47 ransduction inhibitors - that target the bcr-abl oncogene have the potential to render such transplan

48 nd quantify known point mutations in the BCR-ABL oncogene in patients with chronic myelogenous leukem

49 Increased tyrosine kinase activity of abl oncogene in Philadelphia chromosome positive-leukemi

50 n lymphoblastic cells transformed by the BCR/ABL oncogene in response to BCR/ABL tyrosine kinase inhi

51 Expression of either the BCR-ABL or the v-abl oncogene in the factor-dependent murine myeloid cell

52 of the product of the Ph chromosome, the BCR/ABL oncogene, in mice by retroviral bone marrow transduc

53 The Bcr-abl oncogene induces hematopoietic cell transformation a

54 ative stress in cells transformed by the BCR-ABL oncogene is associated with increased DNA double-str

55 sformation of hematopoietic cells by the BCR/ABL oncogene is caused by perturbation of signal transdu

56 tic stem cell disorder in which an activated ABL oncogene is expressed and has been shown to play an

57 type of hematological neoplasm induced by an abl oncogene is influenced not only by what type of hema

58 emia and acute lymphocytic leukemia, the bcr-abl oncogene is involved in this process.

59 The tyrosine kinase activity of the Bcr/Abl oncogene is required for transformation of hematopoi

60 The BCR-ABL oncogene is responsible for most cases of chronic my

61 Our finding, that the P190 BCR/ABL oncogene is still capable of producing leukemia in t

62 various mouse models indicates that the BCR-ABL oncogene is the cause of chronic myeloid leukemia (C

63 otein kinase B (Akt) plays a pivotal role in Abl oncogene-mediated cell survival, we hypothesize that

64 The transforming activity of the v-Abl oncogene of Abelson murine leukemia virus (A-MuLV) i

65 onreceptor tyrosine kinase, encoded by the v-Abl oncogene of Abelson murine leukemia virus induces tr

66 In addition, the v-abl oncogene of Abelson murine leukemia virus, whose pro

67 The v-abl oncogene of the Abelson murine leukemia virus (A-MuL

68 n the Src homology 2 (SH2) domain of the BCR/ABL oncogene on leukemogenesis was tested in a quantitat

69 The bcr-abl oncogene plays a critical role in causing chronic my

70 The bcr-abl oncogene plays a critical role in the pathogenesis o

71 The bcr-abl oncogene, present in 95% of patients with chronic my

72 The BCR/ABL oncogene product is one of the genes associated with

73 In hematopoietic cell lines, the BCR-ABL oncogene product, p210(BCR-ABL), interacts with a va

74 The v-Abl oncogene promotes cell cycle progression and inhibit

75 CML is associated with increased abl oncogene protein tyrosine kinase (PTK) activity.

76 the Abelson leukemia virus derived its Gag-v-Abl oncogene, recent results have linked ABL kinase acti

77 Transfection of each of the three activated ABL oncogenes resulted in rapid emergence of growth fact

78 The BCR/ABL oncogene results from a balanced translocation betwe

79 usly showed that mice expressing an Emicro-v-abl oncogene solely develop plasmacytomas.

80 pression in 32D cells transformed by the bcr-abl oncogene, suggesting that AATYK expression may be a

81 correlated with a specific region of the BCR-ABL oncogene, suggesting that activation (phosphorylatio

82 the appearance of point mutations in the BCR-ABL oncogene that confer resistance to this drug.

83 o/pre-B-cell transformation by v-Abl and BCR-ABL, oncogenes that cause leukemia in mice and humans.

84 In cells harboring the bcr-abl oncogene, the activation (autophosphorylation) of Ca

85 In contrast, after transformation by the BCR/ABL oncogene, the chemotactic response to SDF-1alpha was

86 tion, Lnk deficiency cooperated with the BCR/ABL oncogene, the product of which does not directly int

87 n hematopoietic cells transformed by the BCR/ABL oncogene, this phosphatase complex was found to be c

88 The precise mechanisms by which Abl oncogenes transform hematopoietic cells are unknown.

89 ABL oncogenes trigger multiple signaling pathways whose

90 to compare the biological effects of various ABL oncogenes, we transformed two different factor-depen

91 id leukemia (CML) is the presence of the bcr-abl oncogene, which is associated with transforming abil

92 entified by its presence in the chimeric Bcr/Abl oncogene, which is causative for chronic myeloblasti

93 This drug specifically inhibits the BCR-ABL oncogene, which is required for progression.

94 Meg-01 cells express a p185 BCR/ABL oncogene, which may be responsible for the constitut