Cooperative and redundant effects of STAT5 and Ras signaling in BCR/ABL transformed hematopoietic cells (Q74604694)

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12 November 2019

title

Cooperative and redundant effects of STAT5 and Ras signaling in BCR/ABL transformed hematopoietic cells (English)

1 reference

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12 November 2019

author name string

Hoover RR

1

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12 November 2019

Gerlach MJ

2

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12 November 2019

Koh EY

3

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12 November 2019

Daley GQ

4

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12 November 2019

language of work or name

English

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publication date

1 September 2001

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12 November 2019

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12 November 2019

volume

20

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12 November 2019

issue

41

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12 November 2019

page(s)

5826-5835

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Transduction of interleukin-2 antiapoptotic and proliferative signals via Akt protein kinase

12 November 2019

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The chronic myelogenous leukemia-specific P210 protein is the product of the bcr/abl hybrid gene

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BCR-ABL activates pathways mediating cytokine independence and protection against apoptosis in murine hematopoietic cells in a dose-dependent manner

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Transformation of an interleukin 3-dependent hematopoietic cell line by the chronic myelogenous leukemia-specific P210bcr/abl protein

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STATs and Gene Regulation

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Akt Phosphorylation of BAD Couples Survival Signals to the Cell-Intrinsic Death Machinery

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Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells

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Alternative signals to RAS for hematopoietic transformation by the BCR-ABL oncogene

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Blockade of the Bcr-Abl kinase activity induces apoptosis of chronic myelogenous leukemia cells by suppressing signal transducer and activator of transcription 5-dependent expression of Bcl-xL

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Signaling by the cytokine receptor superfamily

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P210 and P190(BCR/ABL) induce the tyrosine phosphorylation and DNA binding activity of multiple specific STAT family members

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RAS gene mutations in acute and chronic myelocytic leukemias, chronic myeloproliferative disorders, and myelodysplastic syndromes

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Autocrine production and action of IL-3 and granulocyte colony-stimulating factor in chronic myeloid leukemia.

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Multiple tyrosine residues in the cytosolic domain of the erythropoietin receptor promote activation of STAT5.

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The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity

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Tyrosine kinase activity and transformation potency of bcr-abl oncogene products.

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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

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Identification and characterization of a constitutively active STAT5 mutant that promotes cell proliferation

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Il-3-dependent mouse clones that express B-220 surface antigen, contain Ig genes in germ-line configuration, and generate B lymphocytes in vivo.

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Activity of the farnesyl protein transferase inhibitor SCH66336 against BCR/ABL-induced murine leukemia and primary cells from patients with chronic myeloid leukemia

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Bcr-Abl oncoproteins bind directly to activators of the Ras signalling pathway

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Erythropoietin induces activation of Stat5 through association with specific tyrosines on the receptor that are not required for a mitogenic response.

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A requirement for NF-kappa B activation in Bcr-Abl-mediated transformation

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Cooperation between STAT5 and phosphatidylinositol 3-kinase in the IL-3-dependent survival of a bone marrow derived cell line

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Tumorigenic activity of the BCR-ABL oncogenes is mediated by BCL2.

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ras-induced neuronal differentiation of PC12 cells: possible involvement of fos and jun

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Stat5 is essential for the myelo- and lymphoproliferative disease induced by TEL/JAK2

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Fetal anemia and apoptosis of red cell progenitors in Stat5a-/-5b-/- mice: a direct role for Stat5 in Bcl-X(L) induction

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