Innovator resilience potential: A process perspective of individual resilience as influenced by innovation project termination

Innovation projects fail at an astonishing rate. Yet, the negative effects of innovation project failures on the team members of these projects have been largely neglected in research streams that deal with innovation project failures. After such setbacks, it is vital to maintain or even strengthen project members’ innovative capabilities for subsequent innovation projects. For this, the concept of resilience, i.e. project members’ potential to positively adjust (or even grow) after a setback such as an innovation project failure, is fundamental. We develop the second-order construct of innovator resilience potential, which consists of six components – self-efficacy, outcome expectancy, optimism, hope, self-esteem, and risk propensity – that are important for project members’ potential of innovative functioning in innovation projects subsequent to a failure. We illustrate our theoretical findings by means of a qualitative study of a terminated large-scale innovation project, and derive implications for research and management

The MICA-129Met/Val dimorphism affects plasma membrane expression and shedding of the NKG2D ligand MICA.

The MHC class I chain-related molecule A (MICA) is a ligand for the activating natural killer (NK) cell receptor NKG2D. A polymorphism causing a valine to methionine exchange at position 129 affects binding to NKG2D, cytotoxicity, interferon-γ release by NK cells and activation of CD8(+) T cells. It is known that tumors can escape NKG2D-mediated immune surveillance by proteolytic shedding of MICA. Therefore, we investigated whether this polymorphism affects plasma membrane expression (pmMICA) and shedding of MICA. Expression of pmMICA was higher in a panel of tumor (n = 16, P = 0.0699) and melanoma cell lines (n = 13, P = 0.0429) carrying the MICA-129Val/Val genotype. MICA-129Val homozygous melanoma cell lines released more soluble MICA (sMICA) by shedding (P = 0.0015). MICA-129Met or MICA-129Val isoforms differing only in this amino acid were expressed in the MICA-negative melanoma cell line Malme, and clones with similar pmMICA expression intensity were selected. The MICA-129Met clones released more sMICA (P = 0.0006), and a higher proportion of the MICA-129Met than the MICA-129Val variant was retained in intracellular compartments (P = 0.0199). The MICA-129Met clones also expressed more MICA messenger RNA (P = 0.0047). The latter phenotype was also observed in mouse L cells transfected with the MICA expression constructs (P = 0.0212). In conclusion, the MICA-129Met/Val dimorphism affects the expression density of MICA on the plasma membrane. More of the MICA-129Met variants were retained intracellularly. If expressed at the cell surface, the MICA-129Met isoform was more susceptible to shedding. Both processes appear to limit the cell surface expression of MICA-129Met variants that have a high binding avidity to NKG2D.peerReviewe