Figure 5
β2M-specific mAbs abrogate IL-6- and IGF-I-induced signaling pathways. (A) Western blot analysis and (B) densitometric data (AVG) showing protein levels of phosphorylated (p) and nonphosphorylated IL-6R, JAK1, JAK2, STAT3, Akt, Raf, and ERK1/2 in myeloma cells treated with IL-6 (10 ng/mL) or IL-6 together with β2M-specific mAbs (50 μg/mL). (C) Western blot analysis and (D) densitometric data (AVG) showing protein levels of phosphorylated (p) and nonphosphorylated IGF-IRβ, IRS-1, Akt, Raf, and ERK1/2 in myeloma cells treated with IGF-I (50 ng/mL) or IGF-I together with β2M-specific mAbs (50 μg/mL). Results obtained with D1 mAb on MM.1S from 1 representative experiment of 3 performed are shown. Similar results were obtained with other tumor cell lines. Error bars indicate SD.

β2M-specific mAbs abrogate IL-6- and IGF-I-induced signaling pathways. (A) Western blot analysis and (B) densitometric data (AVG) showing protein levels of phosphorylated (p) and nonphosphorylated IL-6R, JAK1, JAK2, STAT3, Akt, Raf, and ERK1/2 in myeloma cells treated with IL-6 (10 ng/mL) or IL-6 together with β2M-specific mAbs (50 μg/mL). (C) Western blot analysis and (D) densitometric data (AVG) showing protein levels of phosphorylated (p) and nonphosphorylated IGF-IRβ, IRS-1, Akt, Raf, and ERK1/2 in myeloma cells treated with IGF-I (50 ng/mL) or IGF-I together with β2M-specific mAbs (50 μg/mL). Results obtained with D1 mAb on MM.1S from 1 representative experiment of 3 performed are shown. Similar results were obtained with other tumor cell lines. Error bars indicate SD.

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