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. 2015 Jun 14;7(5):931–945. doi: 10.1080/19420862.2015.1055442

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© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC

© Eli Lilly and Company

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 3. — Inhibition of IGF-IR-mediated tumor cell signaling and functions by ID2. (A) 100 nM ID2 inhibits IGF-I-induced phosphorylation of IGF-IR, downstream AKT and ERK1/2 in BxPC-3 cells as assessed by immunoblotting analysis. IR mAb and FcD2 were used as controls. (B) 100 nM of ID2 inhibits IGF-I-induced phosphorylation of IGF-IR, downstream AKT and ERK1/2 in MCF-7 cells in immunoblotting analysis. IR mAb and FcD2 were used as controls. (C) Down regulation of surface IGF-IR on MCF-7 cells when treated with ID2, control IR mAb and control human IgG is measured at 0, 1, 4, 8 and 24 hours by IGF-IR electro-chemiluminescence (ECL) assay. (D) ID2 potently inhibits IGF-I induced MCF-7 viability in a dose dependent manner in a CellTiter Glo assay. The error bar represents the SEM from each triplicate measurement.