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BCR — STAT5A

Pathways - manually collected, often from reviews:

• KEGG Pathways in cancer: ABL1/BCR → STAT5A/STAT5B (protein-protein, activation)
• KEGG Chronic myeloid leukemia: ABL1/BCR → STAT5A/STAT5B (protein-protein, activation)
• Reactome Reaction: BCR → STAT5A (reaction) Smedley et al., Neoplasia (New York, N.Y.) 1999*, Heath et al., J Biol Chem 2004*, Chase et al., Blood 2007, Wasag et al., Haematologica 2011*

Text-mined interactions from Literome

Nieborowska-Skorska et al., J Exp Med 1999 (Leukemia) : We show here that BCR/ABL induces phosphorylation and activation of STAT5 by a mechanism that requires the BCR/ABL Src homology (SH)2 domain and the proline-rich binding site of the SH3 domain ... Together, these data demonstrate that STAT5 activation by BCR/ABL is dependent on signaling from more than one domain and document the important role of STAT5 regulated pathways in BCR/ABL leukemogenesis
de Groot et al., Blood 1999 (Cell Transformation, Neoplastic) : STAT5 activation by BCR-Abl contributes to transformation of K562 leukemia cells
Spiekermann et al., Exp Hematol 2002 (Cell Transformation, Neoplastic...) : Stable transfection of BA/F3 cells with TEL-JAK2, TEL-ABL, and BCR-ABL resulted in IL-3 independent growth and strong activation of STAT3 and STAT5 by TEL-JAK2 and TEL-ABL, but not by BCR-ABL
Klejman et al., EMBO J 2002 (Leukemia, Myeloid) : The mechanism of BCR/ABL mediated STAT5 activation is unknown ... Moreover, a kinase-dead Hck mutant and Hck inhibitor PP2 abrogated BCR/ABL dependent activation of STAT5 and elevation of expression of STAT5 downstream effectors A1 and pim-1
Huang et al., Oncogene 2002 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Inhibition of Bcr-Abl kinase activity by PD180970 blocks constitutive activation of Stat5 and growth of CML cells ... Together, these results suggest that the mechanism of action of PD180970 involves inhibition of Bcr-Abl mediated Stat5 signaling and provide further evidence that compounds in this structural class may represent potential therapeutic agents for CML
Zhou et al., J Exp Med 2008 (Cell Transformation, Neoplastic...) : Interestingly, coexpression of Ahi-1 in BCR-ABL-inducible cells reverses growth deficiencies exhibited by BCR-ABL down-regulation and is associated with sustained phosphorylation of BCR-ABL and enhanced activation of JAK2-STAT5
Järås et al., Exp Hematol 2009 : By using a lentiviral anti-signal transducer and activator of transcription 5 ( STAT5 ) short-hairpin RNA, we found that both P190 BCR/ABL1- and P210 BCR/ABL1 induced erythroid cell expansion were STAT5 dependent
Malin et al., Curr Opin Immunol 2010 (Precursor Cell Lymphoblastic Leukemia-Lymphoma) : STAT5 also plays a key role in the generation of B cell precursor acute lymphoblastic leukemia, whereby the BCR-ABL1 translocation or the collaboration of JAK2 mutations with overexpression of the thymic stromal lymphopoietin receptor CRLF2 results in constitutive STAT5 activation leading to cytokine independent survival and growth of leukemic cells
Yuan et al., Blood 2012 (Cell Transformation, Neoplastic...) : In the present study, we show that BCR-ABL activates the expression of the mammalian stress response gene SIRT1 in hematopoietic progenitor cells and that this involves STAT5 signaling
Shuai et al., Oncogene 1996 (Cell Transformation, Neoplastic...) : Reconstitution experiments in non-hematopoietic cells show that STAT5 activation by BCR-ABL occurs independent of cytokines