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Chan, G. C.-F.

Publications and source records attributed to Chan, G. C.-F..

2 recordsLinked to original sources

piRPheno: a manually curated database to prioritize and analyze human disease related piRNAs

Many studies have uncovered that piRNAs (PIWI-interacting RNA) are associated with a broad range of diseases and might be a novel type of biomarkers and targets for precision medicine. However, public resource of high-quality curated human disease-associated piRNAs remains unavailable. Therefore, we developed the piRPheno (http://www.biomedical-web.com/pirpheno) database to provide an up-to-date, interactive and extensible data reference for human piRNA-disease associations. piRPheno includes 9057 experimentally supported associations between 474 piRNAs and 204 diseases through a manual curation of publications. To prioritize the piRNA-disease associations, each association in piRPheno is assigned with a confidence score and clinical correlations based on the experimentally supported evidences. piRPheno is freely available with user-friendly interface and novel applications to enable easy exploration and analysis of the human disease related piRNAs.

bioinformatics↗

Sex differences in gene expression and proliferation are dependent on the epigenetic modifier HP1γ

Sex differences in growth rate in very early embryos have been recognized in a variety of mammals and attributed to sex-chromosome complement effects as they occur before overt sexual differentiation. We previously found that sex-chromosome complement, rather than sex hormones regulates heterochromatin-mediated silencing of a transgene and autosomal gene expression in mice. Here, sex dimorphism in proliferation was investigated. We confirm that male embryonic fibroblasts proliferate faster than female fibroblasts and show that this proliferation advantage is completely dependent upon heterochromatin protein 1 gamma (HP1{gamma}). To determine whether this sex-regulatory effect of HP1{gamma} was a more general phenomenon, we performed RNA sequencing on MEFs derived from males and females, with or without HP1{gamma}. Strikingly, HP1{gamma} was found to be crucial for regulating nearly all sexually dimorphic autosomal gene expression because deletion of the HP1{gamma} gene in males abolished sex differences in autosomal gene expression. The identification of a key epigenetic modifier as central in defining gene expression differences between males and females has important implications for understanding physiological sex differences and sex bias in disease.

developmental biology↗