Can Social Exchange Theory Explain Individual Knowledge-Sharing Behavior? A Meta-Analysis

Motivating people to contribute knowledge has become an important research topic and a major challenge for organizations. In order to promote knowledge-sharing, managers need to understand the mechanism that drives individuals to contribute their valuable knowledge. Several theories have been applied to study knowledge-sharing behavior. However, the research settings and findings are often inconsistent. In this study, we use the social exchange theory as our base to develop an extended model that includes IT support and organizational type as moderators. A meta-analysis on 29 reported studies was conducted to examine how different factors in the social exchange theory affect knowledge-sharing behavior. The findings confirm that the social exchange theory plays an important role underlying individuals’ knowledge-sharing behavior. The results also demonstrate that social interaction and trust derived from the social exchange theory and moderated by IT contextual factors can predict individual’s knowledge-sharing behavior

The Crowding Effect Of Rewards On Knowledge-Sharing Behavior In Virtual Communities

Knowledge sharing is an important activity in virtual communities (VC). Recently, some researchers have explored various motivators that may influence VC members\u27 contribution. Although providing rewards has been found to significantly motivate employees to share knowledge in organizational research, it also has been found to diminish intrinsic motivation and lead to reduced efforts in some cases psychology literature. The phenomenon that external intervention (e.g. monetary incentives or punishments) may either undermine (crowd-out) or enhance (crowd-in) intrinsic motivation is called the motivation crowding effect. Based on the motivation crowding theory, this study investigated the moderating effect of monetary incentives on the relationships of motivations and members\u27 intention for knowledge sharing. The research framework includes two motivational factors, intrinsic and extrinsic motivation, for knowledge sharing in virtual communities. The model was tested using a field experiment on 204 VC members of two different virtual communities. The results confirmed the existence of the crowding effect. That is, the relationship between intrinsic motivation and knowledge sharing intention was significantly lowered after the treatment of monetary incentives. The findings suggest that VC managers should carefully consider providing monetary rewards in promoting their websites because monetary incentives can potentially affect the knowledge-sharing behavior of VC members

The Nuclear Chaperone Nucleophosmin Escorts an Epstein-Barr Virus Nuclear Antigen to Establish Transcriptional Cascades for Latent Infection in Human B Cells

Epstein-Barr Virus (EBV) is an oncogenic γ-herpesvirus that capably establishes both latent and lytic modes of infection in host cells and causes malignant diseases in humans. Nuclear antigen 2 (EBNA2)-mediated transcription of both cellular and viral genes is essential for the establishment and maintenance of the EBV latency program in B lymphocytes. Here, we employed a protein affinity pull-down and LC-MS/MS analysis to identify nucleophosmin (NPM1) as one of the cellular proteins bound to EBNA2. Additionally, the specific domains that are responsible for protein-protein interactions were characterized as EBNA2 residues 300 to 360 and the oligomerization domain (OD) of NPM1. As in c-MYC, dramatic NPM1 expression was induced in EBV positively infected B cells after three days of viral infection, and both EBNA2 and EBNALP were implicated in the transactivation of the NPM1 promoter. Depletion of NPM1 with the lentivirus-expressed short-hairpin RNAs (shRNAs) effectively abrogated EBNA2-dependent transcription and transformation outgrowth of lymphoblastoid cells. Notably, the ATP-bound state of NPM1 was required to induce assembly of a protein complex containing EBNA2, RBP-Jκ, and NPM1 by stabilizing the interaction of EBNA2 with RBP-Jκ. In a NPM1-knockdown cell line, we demonstrated that an EBNA2-mediated transcription defect was fully restored by the ectopic expression of NPM1. Our findings highlight the essential role of NPM1 in chaperoning EBNA2 onto the latency-associated membrane protein 1 (LMP1) promoters, which is coordinated with the subsequent activation of transcriptional cascades through RBP-Jκ during EBV infection. These data advance our understanding of EBV pathology and further imply that NPM1 can be exploited as a therapeutic target for EBV-associated diseases