The influence mechanism of source experience of the knowledge on the knowledge transfer performance: The role of political skill and knowledge barriers.

Exploring the relationship between characteristics of the source of knowledge and knowledge transfer performance seems to be crucial in order to make up for the lack of research on the political skills of knowledge sources in the process of knowledge transfer. For this reason, this study conducts a paired-sample questionnaire survey to achieve the research purpose. One direct supervisor was paired with 1∼4 subordinates; 274 other-reported questionnaires were sent out to supervisors and 1,096 self-reported questionnaires to subordinates. A total of 214 valid supervisor questionnaires and 630 valid subordinate questionnaires were collected. The finding demonstrates that knowledge sources with political skills can reduce knowledge barriers to knowledge transfer as well as affect knowledge transfer performance. This research presents a valid model that comprises the antecedents (characteristics of the knowledge source), mediators (knowledge barriers), moderators (political skill), and consequences of knowledge transfer performance of firms. Moreover, this study provides several meaningful directions for future research.

Anterograde trafficking of KCa3.1 in polarized epithelia is Rab1- and Rab8-dependent and recycling endosome-independent.

The intermediate conductance, Ca2+-activated K+ channel (KCa3.1) targets to the basolateral (BL) membrane in polarized epithelia where it plays a key role in transepithelial ion transport. However, there are no studies defining the anterograde and retrograde trafficking of KCa3.1 in polarized epithelia. Herein, we utilize Biotin Ligase Acceptor Peptide (BLAP)-tagged KCa3.1 to address these trafficking steps in polarized epithelia, using MDCK, Caco-2 and FRT cells. We demonstrate that KCa3.1 is exclusively targeted to the BL membrane in these cells when grown on filter supports. Following endocytosis, KCa3.1 degradation is prevented by inhibition of lysosomal/proteosomal pathways. Further, the ubiquitylation of KCa3.1 is increased following endocytosis from the BL membrane and PR-619, a deubiquitylase inhibitor, prevents degradation, indicating KCa3.1 is targeted for degradation by ubiquitylation. We demonstrate that KCa3.1 is targeted to the BL membrane in polarized LLC-PK1 cells which lack the µ1B subunit of the AP-1 complex, indicating BL targeting of KCa3.1 is independent of µ1B. As Rabs 1, 2, 6 and 8 play roles in ER/Golgi exit and trafficking of proteins to the BL membrane, we evaluated the role of these Rabs in the trafficking of KCa3.1. In the presence of dominant negative Rab1 or Rab8, KCa3.1 cell surface expression was significantly reduced, whereas Rabs 2 and 6 had no effect. We also co-immunoprecipitated KCa3.1 with both Rab1 and Rab8. These results suggest these Rabs are necessary for the anterograde trafficking of KCa3.1. Finally, we determined whether KCa3.1 traffics directly to the BL membrane or through recycling endosomes in MDCK cells. For these studies, we used either recycling endosome ablation or dominant negative RME-1 constructs and determined that KCa3.1 is trafficked directly to the BL membrane rather than via recycling endosomes. These results are the first to describe the anterograde and retrograde trafficking of KCa3.1 in polarized epithelia cells.