Scaffold proteins regulate intracellular MAP kinase signaling by providing 
critical spatial and temporal specificities. We have shown previously that the 
scaffold protein MEK1 partner (MP1) is localized to late endosomes by the 
adaptor protein p14. Using conditional gene disruption of p14 in livers of mice 
(p14(Δhep) ) we analyzed protein and transcript signatures in tissue samples. 
Further biological network analysis predicted that the differentially expressed 
transcripts and proteins are involved in cell cycle progression and regulation 
of cellular proliferation. Although some of the here identified signatures were 
previously linked to phospho-ERK activity, most of them were novel targets of 
the late endosomal p14/MP1/MEK/ERK signaling module. Finally, the proliferation 
defect was confirmed in a chemically induced liver regeneration model in 
p14(Δhep) knockout mice.