2 research outputs found

    Study of virtualness, task interdependence, extra-role performance and team climate in Indian software development teams

    Full text link
    The paper studies the effect of virtualness on team climate and extra-role performance of team members and the moderating effect of task interdependence in this relationship. The sample consists of 125 team members from 25 software development teams. Virtualness index (developed for this study), Team climate inventory (Anderson & west, 1994), task interdependence scale (Pearce & Gregersen, 1991) and Organizational Citizenship Behaviour (OCB) (Podsakoff & MacKenzie 1989) scale were used for measurement. Correlation analysis and 3x2 ANOVA were used for analysis. Results showed that virtualness negatively affected the following variables: a) all the dimensions of vision scale of TCI, b) interaction frequency and influence dimensions of participatory safety scale (TCI) and c) generalized compliance dimension of OCB. Though task interdependence had a significant main effect on OCB and team climate, it did not have any moderating effect

    SIRT3 Blocks Aging-Associated Tissue Fibrosis in Mice by Deacetylating and Activating Glycogen Synthase Kinase 3β.

    Full text link
    Tissue fibrosis is a major cause of organ dysfunction during chronic diseases and aging. A critical step in this process is transforming growth factor 1 (TGF-1)-mediated transformation of fibroblasts into myofibroblasts, cells capable of synthesizing extracellular matrix. Here, we show that SIRT3 controls transformation of fibroblasts into myofibroblasts via suppressing the profibrotic TGF-1 signaling. We found that Sirt3 knockout (KO) mice with age develop tissue fibrosis of multiple organs, including heart, liver, kidney, and lungs but not whole-body SIRT3-overexpressing mice. SIRT3 deficiency caused induction of TGF-1 expression and hyperacetylation of glycogen synthase kinase 3 (GSK3) at residue K15, which negatively regulated GSK3 activity to phosphorylate the substrates Smad3 and -catenin. Reduced phosphorylation led to stabilization and activation of these transcription factors regulating expression of the profibrotic genes. SIRT3 deacetylated and activated GSK3 and thereby blocked TGF-1 signaling and tissue fibrosis. These data reveal a new role of SIRT3 to negatively regulate aging-associated tissue fibrosis and discloses a novel phosphorylation-independent mechanism controlling the catalytic activity of GSK3. Fibrosis
    corecore