Greater visual averaging of face identity for own-gender faces

Recent evidence suggests that observers can rapidly form an average representation based on a set of simultaneously presented faces. Here, we replicate this finding and show that the tendency to process sets of faces in terms of an average representation is greater for own-gender faces. Male and female participants viewed sets of four male or female faces before deciding whether or not a subsequently presented single test face had been present in the set. Incorrect endorsement that it was one of the set members was greater when the test face was a morphed average of the four faces than when it was an actual set member, and this effect was strongest when the gender of the faces was the same as the observer’s. The finding that observers were more likely to incorrectly endorse own-gender (vs. other-gender) faces forms an exception to the often reported own-gender advantage in face recognition

Alternative-splicing defects in cancer: Splicing regulators and their downstream targets, guiding the way to novel cancer therapeutics.

Defects in alternative splicing are frequently found in human tumors and result either from mutations in splicing-regulatory elements of specific cancer genes or from changes in the regulatory splicing machinery. RNA splicing regulators have emerged as a new class of oncoproteins and tumor suppressors, and contribute to disease progression by modulating RNA isoforms involved in the hallmark cancer pathways. Thus, dysregulation of alternative RNA splicing is fundamental to cancer and provides a potentially rich source of novel therapeutic targets. Here, we review the alterations in splicing regulatory factors detected in human tumors, as well as the resulting alternatively spliced isoforms that impact cancer hallmarks, and discuss how they contribute to disease pathogenesis. RNA splicing is a highly regulated process and, as such, the regulators are themselves tightly regulated. Differential transcriptional and posttranscriptional regulation of splicing factors modulates their levels and activities in tumor cells. Furthermore, the composition of the tumor microenvironment can also influence which isoforms are expressed in a given cell type and impact drug responses. Finally, we summarize current efforts in targeting alternative splicing, including global splicing inhibition using small molecules blocking the spliceosome or splicing-factor-modifying enzymes, as well as splice-switching RNA-based therapeutics to modulate cancer-specific splicing isoforms. This article is categorized under: RNA in Disease and Development \u3e RNA in Disease RNA Processing \u3e Splicing Regulation/Alternative Splicing