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Biomedical subjects

Yumiko Sakamoto

Publications and source records attributed to Yumiko Sakamoto.

3 recordsLinked to original sources

I thought we could be friends, but ...: systematic miscommunication and defensive distancing as obstacles to cross-group friendship formation.

This study examined the precursors and consequences of systematic miscommunications regarding relationship interest during intergroup interaction. Pairs of previously unacquainted same-sex students (White-White, White-Chinese, or Chinese-Chinese) engaged in a relatively intimate controlled interaction. White participants who had had little prior contact with Chinese persons were more apt to exhibit a signal-amplification bias (i.e., to perceive that their overtures had conveyed more interest than was actually the case) in intergroup as compared with intragroup exchanges. In contrast, White participants with high levels of prior contact with Chinese persons and Chinese participants did not show enhanced signal amplification in intergroup relative to intragroup exchanges. These results support our hypothesis that lack of intergroup contact experience sets the stage for miscommunications regarding friendship interest. White participants' tendency to feel that they had initially communicated more interest in being friends than their Chinese partner mediated a downward shift in their actual friendship interest over time, suggesting that signal amplification triggers defensive distancing and ultimately lowers the likelihood of cross-group friendship formation.

Adult↗

Polyhistidine tract expansions in HOXA1 result in intranuclear aggregation and increased cell death.

HOXA1 gene is part of a cluster of homeotic selector genes that regulates the anteroposterior patterning of mammals during embryonic development. HOXA1 encodes two alternatively spliced mRNAs with two isoforms, A and B, the former contains the homeodomain and expressed in early embryonic development. HOXA1 contains a string of 10 histidine repeats. However, individuals heterozygous for 7, 9, 11, and 12 histidine repeat variants were present among the Japanese population, notably in some autism cases. To determine the biological implications of the different polyhistidine repeat lengths, we expressed these variants in COS-7 and a human neuroblastoma cell line (SK-N-SH). Expression of expanded variants of HOXA1 isoform A, containing 11 and 12 polyhistidine, resulted in early and great degree of protein aggregation in the nucleus. This aggregation resulted in accelerated cell death in cells expressing 11 and 12 expanded variants compared to those transfected with 7 and 10 polyhistidine variants. Furthermore, we showed that these aggregates were ubiquitinated and were inhibited by a histidine-modifying compound, DEPC. These data suggest that HOXA1 protein with polyhistidine tract expansions misfold, aggregate, and have a toxic effect on cell.

Animals↗