BCR-ABL fails to inhibit apoptosis in U937 myelomonocytic cells expressing a carboxyl-terminal truncated STAT5

Leukemia and Lymphoma

Volumn 42, Issue 3, 2001, Pages 445-455

  Ahmed, M ^a   Dusanter Fourt, I ^a   Dugray, A ^a   Dubrez, L ^a   Novault, S ^a   Bonnet, M L ^a   Gisselbrecht, S ^a   Varet, B ^a   Solary, E ^a   Vainchenker, W ^a   Turhan, A G ^a  

^a INSTITUT GUSTAVE ROUSSY   (France)

Author keywords

BCR ABL; Carboxyl terminal truncated STATS; Inhibition of apoptosis; Myelomonocytic cells; U937 cells

Indexed keywords

BCR ABL PROTEIN; CERAMIDE; CYTOKINE; ETOPOSIDE; FAS LIGAND; GAMMA INTERFERON; GRANULOCYTE MACROPHAGE COLONY STIMULATING FACTOR; GROWTH FACTOR; PROTEIN ANTIBODY; PROTEIN BAX; STAT PROTEIN; STAT1 PROTEIN; STAT5 PROTEIN; TUMOR NECROSIS FACTOR; VIRUS VECTOR;

AMINO TERMINAL SEQUENCE; APOPTOSIS; ARTICLE; ASSAY; CARBOXY TERMINAL SEQUENCE; CELL CLONE; CELL LINE; CELL STRAIN U937; CONTROLLED STUDY; CROSS LINKING; GENE EXPRESSION; HEMATOPOIETIC CELL; HUMAN; HUMAN CELL; KINETICS; MOLECULE; MONOCYTE; PRIORITY JOURNAL; PROMYELOCYTE; PROTEIN EXPRESSION; RETROVIRUS; SERUM; SIGNAL TRANSDUCTION;

EID: 0034908521     PISSN: 10428194     EISSN: None     Source Type: Journal    
DOI: 10.3109/10428190109064601     Document Type: Article

References (45)

1. Inhibition of apoptosis by BCR-ABL in chronic myeloid leukemia
2. Structural and signaling requirements for BCR-ABL mediated transformation and inhibition of apoptosis
3. BCR-ABL and constitutively active erythropoietin receptor (cEpoR) activate distinct mechanisms for growth factor-independence and inhibition of apoptosis in Ba/F3 cell line
4. Apoptosis in chronic myeloid leukaemia: Normal responses by progenitor cells to growth factor deprivation, X-irradiation and glucocorticoids
5. Primary proliferating immature myeloid cells from CML patients are not resistant to induction of apoptosis by DNA damage and growth factor withdrawal
6. Apoptosis in chronic myelogenous leukemia: Studies of stage-specific differences
7. Bcr-abl oncogenes renders myeloid cell line factor independent: Potential autocrine mechanisms in chronic myeloid leukemia
8. Expression of bcr-abl abrogates factor-dependent growth of human hematopoietic M07E cells by an autocrine mechanism
9. Bcr-Abl oncoproteins bind directly to activators of the Ras signalling pathway
10. p130CAS forms a signaling complex with the adapter protein CRKL in hematopoietic cells transformed by the BCR/ABL oncogene
11. Regulation of the Fas apoptotic cell death pathway by Abl
12. Bcr-Abl exerts its antiapoptotic effect against diverse apoptotic stimuli through blockage of mitochondrial release of cytochrome C and activation of caspase-3
13. Versatile retroviral vectors for potential use in gene therapy
14. BCR-ABL delays apoptosis upstream procaspase-3 activation
15. Interleukin-3, erythropoietin, and prolactin activate a STAT5-like factor in lymphoid cells
16. Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl
17. Constitutive activation of STAT5 by the BCR-ABL oncogene in chronic myelogenous leukemia
18. P210 and P190(BCR/ABL) induce the tyrosine phosphorylation and DNA binding activity of multiple specific STAT family members
19. Prolactin, growth hormone, erythropoietin and granulocyte-macrophagecolony stimulating factor induce MGF-StatS DNA binding activity
20. Tumorigenic activity of the BCR-ABL oncogenes is mediated by BCL2
21. Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery
22. Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway
23. Expression of constitutively active Raf-1 in the mitochondria restores antiapoptotic and leukemogenic potential of a transformation-deficient BCR/ABL mutant
24. The BCR-ABL tyrosine kinase inhibits apoptosis by activating a Ras-dependent signaling pathway
25. A requirement for NF-kappaB activation in Bcr-Abl-mediated transformation
26. Activation of the Jak2-Stat5 signaling pathway in Nb2 lymphoma cells by an anti-apoptotic agent, aurintricarboxylic acid
27. Stat3 activation is responsible for IL-6-dependent T cell proliferation through preventing apoptosis: Generation and characterization of T cell-specific Stat3-deficient mice
28. STATs as activators of apoptosis
29. BCR/abl leads to the constitutive activation of Stat proteins, and shares an epitope with tyrosine phosphorylated Stats
30. Constitutive activation of JAKs and STATs in BCR-Abl-expressing cell lines and peripheral blood cells derived from leukemic patients
31. Functionally distinct isoforms of STAT5 are generated by protein processing
32. Carboxyl-truncated STAT5beta is generated by a nucleus-associated serine protease in early hematopoietic progenitors
33. Identification of an additional isoform of STAT5 expressed in immature macrophages
34. Signal transducer and activator of transcription (STAT)5 activation by BCR/ABL is dependent on intact Src homology (SH)3 and SH2 domains of BCR/ABL and is required for leukemogenesis
35. Suppression of interleukin-3-induced gene expression by a C-terminal truncated Stat5: Role of Stat5 in proliferation
36. Regulation of cell growth by IL-2: Role of STAT5 in protection from apoptosis but not in cell cycle progression
37. Heteromerization of the gammac chain with the interleukin-9 receptor alpha subunit leads to STAT activation and prevention of apoptosis
38. Anti-apoptotic signals of granulocyte-macrophage colony-stimulating factor are transduced via Jak2 tyrosine kinase in eosinophils
39. STAT3 mediates the survival signal in oncogenic ras-transfected intestinal epithelial cells
40. Positive selection of apoptosis-resistant cells correlates with activation of dominant-negative STAT5
41. Granulocyte-macrophage colony-stimulating factor induces a unique set of STAT factors in murine dendritic cells
42. The structure, regulation and function of the Janus kinases (JAKs) and the signal transducers and activators of transcription (STATs)
43. A family of serine proteases expressed exclusively in myelo-monocytic cells specifically processes the nuclear factor-kappa B subunit p65 in vitro and may impair human immunodeficiency virus replication in these cells
44. Detection of major bcr-abl gene expression at a very low level in blood cells of some healthy individuals
45. The presence of typical and atypical BCR-ABL fusion genes in leukocytes of normal individuals: Biologic significance and implications for the assessment of minimal residual disease