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. 2018 Jan 5;17(3):4422–4432. doi: 10.3892/mmr.2018.8383

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Copyright: © Li et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 11. — The ERK signaling pathway. (A) shows that high doses of arsenic for a short period of time enhances Ras, Raf, MEK and ERK phosphorylation in normal cells, thereby the activated ERK translocates from cytoplasm into nucleus, increases levels of Bax protein, decreases levels of Bcl-2 protein and cleaves caspase-3, contributing to cell apoptosis. (B) indicates that, in cancer cells, low dose arsenic intervention for long period of time suppresses phosphorylation of Ras, Raf, MEK and ERK, blocking ERK translocation from cytoplasm into nucleus, thereby increases levels of Bax protein, decreases levels of Bcl-2 protein and cleaves caspase-3, contributing to cell apoptosis. ERK, extracellular signal-regulated MAP kinases; MEK, mitogen-induced extracellular kinase; p-ERK, phosphorylated extracellular signal-regulated kinase; Raf, serine/threonine-specific protein kinases; Bcl-2, B-cell lymphoma/leukemia-2 protein; Bax, Bcl-associated X protein; caspase-3, cysteinyl aspartate-specific protease-3; RTKs, receptor tyrosine kinases.

Figure 11. — The ERK signaling pathway. (A) shows that high doses of arsenic for a short period of time enhances Ras, Raf, MEK and ERK phosphorylation in normal cells, thereby the activated ERK translocates from cytoplasm into nucleus, increases levels of Bax protein, decreases levels of Bcl-2 protein and cleaves caspase-3, contributing to cell apoptosis. (B) indicates that, in cancer cells, low dose arsenic intervention for long period of time suppresses phosphorylation of Ras, Raf, MEK and ERK, blocking ERK translocation from cytoplasm into nucleus, thereby increases levels of Bax protein, decreases levels of Bcl-2 protein and cleaves caspase-3, contributing to cell apoptosis. ERK, extracellular signal-regulated MAP kinases; MEK, mitogen-induced extracellular kinase; p-ERK, phosphorylated extracellular signal-regulated kinase; Raf, serine/threonine-specific protein kinases; Bcl-2, B-cell lymphoma/leukemia-2 protein; Bax, Bcl-associated X protein; caspase-3, cysteinyl aspartate-specific protease-3; RTKs, receptor tyrosine kinases.