It is proposed that property transmission becomes a general and readily available hypothesis used to make
interpretations and judgments about causal questions under conditions of uncertainty, in which property transmission functions as a heuristic. VX-765 cost The property transmission hypothesis explains why and when similarity information is used in causal inference. It can account for magical contagion beliefs, some cases of illusory correlation, the correspondence bias, overestimation of cross-situational consistency in behavior, nonregressive tendencies in prediction, the belief that acts of will are causes of behavior, and a range of other phenomena. People learn that property transmission is often moderated by other factors, but under conditions of uncertainty in which the operation of relevant other factors is unknown, it tends to exhibit a pervasive influence on thinking about causality.”
“Previous studies characterized two types of replication-defective human immunodeficiency virus type 1 (HIV-1) integrase mutants: class I, which are specifically blocked at the integration step, and class II, which harbor additional virion production and/or reverse transcription defects. Class
I mutant enzymes supported little AZD6244 ic50 if any metal ion-dependent 3 ‘-processing and DNA strand transfer activities in vitro, whereas class II enzymes displayed partial or full catalytic function in studies with simplified assay designs, suggesting that defective interaction(s) with heterologous integrase binding proteins might underlie the class II mutant viral phenotype. To address this hypothesis, Rucaparib class I and II mutant enzymes were interrogated under
expanded sets of in vitro conditions. The majority failed to catalyze the concerted integration of two viral DNA ends into target DNA, highlighting defective integrase function as the root cause of most class II in addition to all class I mutant virus infection defects. One mutant protein, K264E, in contrast, could support the wild-type level of concerted integration activity. After accounting for its inherent reverse transcription defect, HIV-1(K264E) moreover formed preintegration complexes that supported the efficient integration of endogenous viral DNA in vitro and normal levels and sequences of 2-long terminal repeat-containing circle junctions during acute infection. K264E integrase furthermore efficiently interacted in vitro with two heterologous binding partners, LEDGF/p75 and reverse transcriptase. Our results underscore the physiological relevance of concerted integration assays for tests of integrase mutant function and suggest that the K264E mutation disrupts an interaction with an intranuclear integrase binding partner that is important for HIV-1 integration.