Figure 1.
Nicotine: activation of cell proliferation. In quiescent cell there is the absence of the association between β-annexin, src and nAchR. Rb is dephoshorylated and binds the transcription factor E2F which, as a consequence, cannot be active on cell proliferation. The binding of nicotine to its receptor nAcR induces formation of a holigomeric complex between β-annexin, src and nAchR. The latter activates MAPKs activation and in detail the binding of BRAF and the complex RB-E2F. Undetermined mitogenic stimuli (e.g., cyclins) can enable the E2F transcription factor to act on gene promoters and lead the cell to the phase S of the cell cycle. The increase of intracellular calcium levels which is consequent to nicotine binding to the nAchR promote the activation of ERK signaling. As a consequence EKK1 activates the transcription factor NFκB which sustains cell proliferation
