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CD79B — STAT5A

Text-mined interactions from Literome

Nieborowska-Skorska et al., J Exp Med 1999 (Leukemia) : 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
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
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