Digital channels have been rising to the major shopping paths from the past few years, yet it is interesting to notice that more and more digital retailers advance into offline channel nowadays due to the benefits. For example, the digital retailing giant Amazon opened its first bricks-and-mortar bookstore in 2015. Dell, which distributes its products only in the catalog and digital channels, entered the leading retail stores such as Best Buy and Walmart. The digital retailers’ strategy trend that moves into the real world reveals the unique and powerful capabilities of the offline distribution channel and the importance of launching products in the offline channel. Previous studies in marketing have investigated various complement and substitute impacts of offline channel introduction (i.e., Avery et al. 2012, Wang and Goldfarb 2017). However, most of the literature focus on the pc-based online channel and catalog, there is little research about the impact of offline channel introduction on smartphone-based mobile channel. Although mobile channel is similar to online channel in many ways (i.e., internet access and convenient shopping), it can be distinguished from online channel in terms of search and access, leading to a different interplay with offline channel. This research, therefore, aims to investigate how product launching in offline channel affects purchases in mobile channel versus online channel, and deepen the understanding by exploring the moderating effect of offline store intensity. Besides, we also explore the interaction between two digital channels: online channel and mobile channel. As most of the multi-channel retailers offer products in both online and mobile channels, it is incremental to know the interplay between these two digital channels. Using data from a representative multichannel retailer selling beauty products, we find the following three empirical results. First, product introduction in offline channel has a positive effect on online and mobile sales, and the effect is greater for mobile. Second, as offline store increases, the positive impact of offline product launch weakens on online channel, and even turns to negative once the number of offline stores reaches a threshold. However, the influence on mobile channel stays the same. The results reflect that the complementary interplay between offline and mobile channel is relatively stronger than between online channel. Finally, within the digital channels, online purchases only increase with the growth of sales performance within online channel, whereas mobile purchases are positively affected by both within mobile channel sales and across online channel sales. Our findings contribute critical academic and managerial implications for multichannel retailing.

The diffe rentiation of osteoblasts from mesenchymal precursors requires a series of cell fa te decis ions controlled by a hi erarchy of transcription factors Among these are RUNX2, osterix (OSX) , ATF4 and a la rge number of nuclear co-regulators. During bone development, initial RUNX2 expression coincides with the formation of mesenchyma l con densations well before the branching of chondrogenic and osteogenic lineages. Runx2 is s ubject to a number 0 1' post - tran scriptional controls including regulation by nuclear accessory factors such as ATF4 and DLX5 and post-trans lational mod ificati on, especially phosphOl‘ylation. We previously showed that Runx2-dependent transcription is acti vated by the ex tracellular signal-regulated/MAP kinase pathway in response to ECM/integrin and FGF2 stimulation. To identify and a5sess the function of ERK/MAPK phosphorylation s ites in RUNX2 and esta bli sh the role of MAPK s ignaling in bone fo 1'mation Approaches: A deletion/mutagenesis approach wa5 used to ide ntify 1'egions 0 1' RUNX2 necessary fo1' MAPK responsiveness and phosphorylation. To evaluate the in vivo function of the ERK/MAPK pa thway‘ transgen ic mice were developed wi th osteoblast- specific expression of either dominant-negative 0 1' cons titutively-active MEKl in osteoblasts and crossed with Runx2 heterozygous-• null ammals RUNX2 is phosphorylated on two critical serine res idues in the P/S/T domain. RUNX2 conta ining S/A mutations in these sites is refractory to MAPK stimula ti on while S/E muta tions cause cons titutive activation MAPK activation of RUNX2 was also found to occur in vivo 까'a n sge ni c expression of cons titutively ac tive MEKl in osteo • blas ts accelerated skeletal development while a dominant-negati ve MEKl reta rd ed bone formation in a RUNX2- dependent manner As shown by these studies‘ the ERK/MAPK pathway controls Runx2 tra nscript iona l activ ity by phosphorylation at specific serine residues. This may be a major pathway for controlling osteoblast activity in response to extracellul ar matrix signals. mechanical loads and hormonal stimulation