ライフサイエンスコーパス: abl gene

1 of a primitive hematopoietic cell by the BCR/ABL gene.

2 on on Bcr-Abl TK or amplification of the bcr-abl gene.

3 e identified in the kinase domain of the BCR/ABL gene.

4 kemogenic by transfection with the human BCR/ABL gene.

5 inhibits the ABL kinase activity of the BCR-ABL gene.

6 ein associated with amplification of the BCR-ABL gene.

7 BCR gene are fused to a large portion of the ABL gene.

8 evels comparable to that of the endogenous c-abl gene.

9 of a primitive hematopoietic cell by the BCR/ABL gene.

10 r the immunodeficiency in mice lacking the c-abl gene.

11 ls expressing either wild-type or mutant BCR/ABL genes.

12 ransformation by derivatives of the Abelson (abl) gene.

13 Mice carrying homozygous mutations in the c-abl gene (abl-(m1) or abl2) exhibit severe, though varia

14 Cells lacking the c-abl gene also responded to ara-C and MMS with increases

15 undergo detectable amplification of the BCR/ABL gene, although they displayed a 2-fold to 3-fold inc

16 ercame imatinib resistance in cells with Bcr-Abl gene amplification.

17 sistance was associated with progressive BCR-ABL gene amplification.

18 increase in the number of copies of the BCR/ABL gene and its level of expression.

19 1) elucidate the mechanisms by which the BCR-ABL gene and its product initiate and maintain the malig

20 in LasBD can suppress expression of the BCR/ABL gene and restore normal function of BCR/ABL cDNA-con

21 amplification and overexpression of the BCR-ABL gene and the emergence of mutant isoforms of BCR-ABL

22 ing after injection of CP cells lacked a BCR-ABL gene and were presumably normal.

23 The Ph-translocation joins the BCR and ABL genes and leads to expression of a chimeric Bcr/Abl

24 cular abnormalities caused by the hybrid Bcr-Abl gene are causally associated with the development an

25 egative c-Abl mutant and cells lacking the c-abl gene are impaired in their ability to downregulate C

26 Mutant forms of the c-ABL gene are well known to be involved in hematopoietic

27 ant phenotype, 2) improve the use of the BCR-ABL gene as a diagnostic marker of disease, and 3) inhib

28 on of the p210 and the p190 types of the BCR-ABL gene associated with chronic myeloid leukemia (CML)

29 he fusion of 5' parts of the BCR gene to the ABL gene at the second exon yields several forms of an o

30 region and fusion between the BCR and the c-ABL genes (BCR-ABL) oncogen product is a potential tumor

31 ditionally, genomic amplification of the BCR-ABL gene can occasionally be detected.

32 ming cells but only in a fraction of the BCR/ABL gene copies in each cell.

33 0% of the BCR/ABL transcripts and 10% of BCR/ABL gene copies on the DNA level were mutated.

34 d by reduced Khc gene dosage, a reduction in Abl gene dosage caused distal paralysis and axonal swell

35 Our study suggests important roles of BCR-ABL gene expression and its native chromosomal locus for

36 genous leukemia patients with continuous BCR-ABL gene expression but undetectable BCR-ABL protein exp

37 mutant Bcr/Abl protein without affecting bcr/abl gene expression in chronic myelogenous leukemia (CML

38 , which are rendered IL-3 independent by BCR-ABL gene expression.

39 f enhanced expression or mutation of the BCR-ABL gene has been detected in patients.

40 nonreceptor tyrosine kinase encoded by the c-Abl gene has the unique feature of an F-actin binding do

41 lls that are stably transfected with the bcr-abl gene (HL-60/Bcr-Abl) and express p185 Bcr-Abl; and (

42 ession of a 5'-UTR-deleted mutant of the bcr-abl gene, i.e., Jurkat/Bcr-Abl (5'UTR-) cells.

43 Sequencing of the BCR-ABL gene in patients who have relapsed after STI-571 che

44 Expression of the BCR/abl gene induces hematologic malignancies in transgenic

45 re different depending on whether the raf or abl gene is present in myc-containing viruses.

46 Formation of the hybrid BCR-ABL gene is responsible for >95% of chronic myeloid leuk

47 2 that fuses coding sequences of the Bcr and Abl genes is responsible for a remarkably diverse group

48 genes, BCR and ABL, to form an aberrant BCR-ABL gene on chromosome 22.

49 inigenes encode the two major forms of the c-abl gene product (c-Abl types I and IV) and a kinase def

50 ot require binding of p85 SH2 domains to BCR/abl gene product and involves interaction with other tyr

51 The BCR/ABL gene product of the Philadelphia (Ph) chromosome ind

52 at either of the two alternatively spliced c-abl gene products can provide the in vivo functions of c

53 ata demonstrate that although both activated abl gene products promote overlapping effects of some bi

54 TC-IC and the presence or absence of the BCR/ABL gene rearrangement in progeny of primitive LTC-IC.

55 The BCR-ABL gene rearrangement, the initial event in the develop

56 an hematopoietic stem cell caused by the BCR/ABL gene rearrangement.

57 nding site mutations or amplification of Bcr-Abl gene, resulting in a Bcr-Abl tyrosine kinase that is

58 Abnormal fusion of the BCR and ABL genes, resulting from the formation of the Philadelp

59 inadvertent fusion of the bcr gene with the abl gene results in a constitutively active tyrosine kin

60 curred most rapidly in the p16, PAX-6, and c-ABL genes, shown to be transcribed prior to drug treatme

61 CML patients possess a fused BCR-ABL gene that activates the Abl tyrosine kinase domain w

62 epends on the number of mutations in the BCR-ABL gene that confer resistance to the drugs, as well as

63 We expressed a kinase-inactive BCR/ABL gene to directly investigate the role of kinase acti

64 temperature-sensitive mutant of the p210 BCR-ABL gene, transfected into a growth factor-dependent cel

65 is induced in 32D cells transformed by the v-abl gene when these cells are incubated in the presence

66 Expression of BCR/ABL genes with deletions of either the COOH-terminal act