Differences between risk perception and risk-taking are related to impulsivity levels.

Background: Although there is broad agreement that perceived risks determine risk-taking behavior, previous research has shown that this association may not be as straightforward as expected. The main objective of this study was to investigate if the levels of impulsivity can explain part of these controversial findings. Method: A total of 1579 participants (Mage = 23.06, from 18 to 60 years; 69.4% women) were assessed for levels of risk perception, risk-taking avoidance, and impulsivity. Results: The results showed that while impulsivity was significantly and negatively related to both risk perception and risk-taking avoidance, the relationship with risk-taking avoidance was significantly stronger than with risk perception. The levels of impulsivity predicted risk-taking avoidance even when controlling for risk perception. Conclusions: These findings indicate that impulsivity can differentially affect risk perception and risk-taking. We propose that the stronger influence of impulsivity on risk-taking is due to the greater reliance of risk-taking, compared with risk perception, on automatic processes guided by impulses and emotions.

The leukemogenic AF4-MLL fusion protein causes P-TEFb kinase activation and altered epigenetic signatures.

Expression of the AF4-MLL fusion protein in murine hematopoietic progenitor/stem cells results in the development of proB acute lymphoblastic leukemia. In this study, we affinity purified the AF4-MLL and AF4 protein complexes to elucidate their function. We observed that the AF4 complex consists of 11 binding partners and exhibits positive transcription elongation factor b (P-TEFb)-mediated activation of promoter-arrested RNA polymerase (pol) II in conjunction with several chromatin-modifying activities. In contrast, the AF4-MLL complex consists of at least 16 constituents including P-TEFb kinase, H3K4(me3) and H3K79(me3) histone methyltransferases (HMT), a protein arginine N-methyltransferase and a histone acetyltransferase. These findings suggest that the AF4-MLL protein disturbs the fine-tuned activation cycle of promoter-arrested RNA Pol II and causes altered histone methylation signatures. Thus, we propose that these two processes are key to trigger cellular reprogramming that leads to the onset of acute leukemia.