Earlier findings suggest that positions of power decrease self-other integration and increase psychological distance to others. Until now, however, evidence for this relation rests exclusively on... Show moreEarlier findings suggest that positions of power decrease self-other integration and increase psychological distance to others. Until now, however, evidence for this relation rests exclusively on subjective measures. The current research instead employed a vertical joint Simon task to measure self-other integration. This task assesses the extent to which people represent their own actions in reference to their co-actor's, also referred to as the joint Simon effect. Building on cultural associations between power and vertical elevation, we manipulated whether participants were in an elevated (high-power) or lower (low-power) seating position. Experiments 1a and 1b reanalyzed existing datasets and found that elevated (vs. lower) seating position decreased the joint Simon effect, consistent with predictions. Experiment 2 provides a high-powered replication of this finding. Yet, further analyses revealed that feelings of power – measured as a manipulation check and indeed demonstrating that the manipulation was successful – did not mediate or moderate the effect of seating position on the joint Simon effect. Therefore, it is possible that the effect of seating elevation was driven through other aspects of that manipulation than feelings of power. We discuss these and suggest ways to test these alternative explanations. Show less
The p53 regulatory network is critically involved in preventing the initiation of cancer. In unstressed cells, p53 is maintained at low levels and is largely inactive, mainly through the action of... Show moreThe p53 regulatory network is critically involved in preventing the initiation of cancer. In unstressed cells, p53 is maintained at low levels and is largely inactive, mainly through the action of its two essential negative regulators, HDM2 and HDMX. p53 abundance and activity are up-regulated in response to various stresses, including DNA damage and oncogene activation. Active p53 initiates transcriptional and transcription-independent programs that result in cell cycle arrest, cellular senescence, or apoptosis. p53 also activates transcription of HDM2, which initially leads to the degradation of HDMX, creating a positive feedback loop to obtain maximal activation of p53. Subsequently, when stress-induced post-translational modifications start to decline, HDM2 becomes effective in targeting p53 for degradation, thus attenuating the p53 response. To date, no clear function for HDMX in this critical attenuation phase has been demonstrated experimentally. Like HDM2, the HDMX gene contains a promoter (P2) in its first intron that is potentially inducible by p53. We show that p53 activation in response to a plethora of p53-activating agents induces the transcription of a novel HDMX mRNA transcript from the HDMX-P2 promoter. This mRNA is more efficiently translated than that expressed from the constitutive HDMX-P1 promoter, and it encodes a long form of HDMX protein, HDMX-L. Importantly, we demonstrate that HDMX-L cooperates with HDM2 to promote the ubiquitination of p53 and that p53-induced HDMX transcription from the P2 promoter can play a key role in the attenuation phase of the p53 response, to effectively diminish p53 abundance as cells recover from stress. Show less
