Fig. 10.
Fig. 10. No qualitative defect in activation of signaling pathways in primary myeloid cells expressing p210 ΔSH2. / Western blotting with the indicated antibodies was performed on extracts from myeloid cells isolated from mice with p210 wild-type–induced (left side) or p210 ΔSH2-induced (right side) CML-like disease. As controls, extract from untransduced Balb/c bone marrow (BM) and from NIH 3T3 cells without (−) and with (+) stimulation with PDGF were included at the far right. Equivalent amounts of total protein were present in each lane as judged by Ponceau S staining of the membrane. (A) Anti–C-terminal Abl antibody. (B) Anti-c-Myc antibody. (C) Antiphospho-STAT5 (top) and anti-STAT5A (bottom). (D) Anti-phospho-Akt (top) and anti-pan-Akt (bottom). (E) Anti-phospho-ERK (top) and anti-pan-ERK (bottom). Both p42 and p44 ERK are detected. (F) Anti-phospho-JNK (top) and anti-pan-JNK (bottom). Both p46 and p54 JNK are detected.

No qualitative defect in activation of signaling pathways in primary myeloid cells expressing p210 ΔSH2.

Western blotting with the indicated antibodies was performed on extracts from myeloid cells isolated from mice with p210 wild-type–induced (left side) or p210 ΔSH2-induced (right side) CML-like disease. As controls, extract from untransduced Balb/c bone marrow (BM) and from NIH 3T3 cells without (−) and with (+) stimulation with PDGF were included at the far right. Equivalent amounts of total protein were present in each lane as judged by Ponceau S staining of the membrane. (A) Anti–C-terminal Abl antibody. (B) Anti-c-Myc antibody. (C) Antiphospho-STAT5 (top) and anti-STAT5A (bottom). (D) Anti-phospho-Akt (top) and anti-pan-Akt (bottom). (E) Anti-phospho-ERK (top) and anti-pan-ERK (bottom). Both p42 and p44 ERK are detected. (F) Anti-phospho-JNK (top) and anti-pan-JNK (bottom). Both p46 and p54 JNK are detected.

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