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This effect appeared to be dose dependant in nature, where low-moderate use had a reduced effect on carcinoma development [37, 42], while higher lifetime use associated a greater risk of malignancy [30, 60]

Furthermore, increased expression of BAG2 shifts the effects of nicotine toward a reduction in levels of p-tau protein, possibly as a consequence of BAG2 inhibition of ERK1/2 via association with Hsp90, which is required for ERK1/2 activity, and/or via BAG2-mediated degradation of p-tau as a consequence of BAG2 phosphorylation by p38/MAPKAPK2 [206]

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