Towards consistent demarcation of enterprise design domains

This article supports the ideology that enterprise engineering (EE) could add more value if EE researchers focus on facilitating effective conversations within design teams to create a common understanding of the enterprise. One way of creating a common understanding is to define and demarcate enterprise design domains in a consistent way. Literature presents different conceptualisations for demarcating design domains, without using a systematic demarcation rationale. As an example, this article introduces Hoogervorst’s approach and associated enterprise design domains to highlight practical difficulties when emerging design principles are applied to four main design domains, as defined by Hoogervorst. Based on the suggestion to apply the basic system design process to demarcate the main enterprise design domains in a consistent way and addressing the need for additional design domains, we present four alternative enterprise design domains, developed via design science research. We also demonstrate the usefulness of the new design domains by presenting several examples of enterprise design cycles that occur during enterprise design.http://link.springer.combookseries/5582018-11-10hj2018Industrial and Systems Engineerin

Prolyl isomerase Pin1 and protein kinase HIPK2 cooperate to promote cortical neurogenesis by suppressing groucho/TLE:Hes1-mediated inhibition of neuronal differentiation

The Groucho/transducin-like Enhancer of split 1 (Gro/TLE1):Hes1 transcriptional repression complex acts in cerebral cortical neural progenitor cells to inhibit neuronal differentiation. The molecular mechanisms that regulate the anti-neurogenic function of the Gro/TLE1:Hes1 complex during cortical neurogenesis remain to be defined. Here we show that prolyl isomerase Pin1 (peptidyl-prolyl cis-trans isomerase NIMA-interacting 1) and homeodomain-interacting protein kinase 2 (HIPK2) are expressed in cortical neural progenitor cells and form a complex that interacts with the Gro/TLE1:Hes1 complex. This association depends on the enzymatic activities of both HIPK2 and Pin1, as well as on the association of Gro/TLE1 with Hes1, but is independent of the previously described Hes1-activated phosphorylation of Gro/TLE1. Interaction with the Pin1:HIPK2 complex results in Gro/TLE1 hyperphosphorylation and weakens both the transcriptional repression activity and the anti-neurogenic function of the Gro/TLE1:Hes1 complex. These results provide evidence that HIPK2 and Pin1 work together to promote cortical neurogenesis, at least in part, by suppressing Gro/TLE1:Hes1-mediated inhibition of neuronal differentiation