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| 1 | Donor HLA‐C Genotype Has a Profound Impact on the Clinical Outcome Following Liver Transplantation显示文摘 | R.Hanvesakul N.Spencer M.Cook B.Gunson M.Hathaway R.Brown P.Nightingale P.Cockwell S. G.Hubscher D. H.Adams P.Moss D.Briggs | 2008 | American Journal of Transplantation2008，，9： | 2 |
| 2 | The human malaria parasite genome is configured into thousands of coexpressed linear regulatory units显示文摘The human malaria parasite Plasmodium falciparum thrives in radically different host environments in mosquitoes and humans, with only a limited set of transcription factors. The nature of regulatory elements or their target genes in the P. falciparum genome remains elusive. Here, we found that this eukaryotic parasite uses an efficient way to maximally use genetic and epigenetic regulation to form regulatory units(RUs) during blood infections. Genes located in the same RU tend to have the same pattern of expression over time and are associated with open chromatin along regulatory elements. To precisely define and quantify these RUs, a novel hidden Markov model was developed to capture the regulatory structure in a genome-wide fashion by integrating expression and epigenetic evidence. We successfully identified thousands of RUs and cross-validated with previous findings. We found more genes involved in red blood cell(RBC) invasion located in the same RU as the Pf AP2-I(AP2-I) transcription factor, demonstrating that AP2-I is responsible for regulating RBC invasion. Our study has provided a regulatory mechanism for a compact eukaryotic genome and offers new insights into the in vivo transcriptional regulation of the P. falciparum intraerythrocytic stage. | Chengqi Wang Justin Gibbons Swamy R.Adapa Jenna Oberstaller Xiangyun Liao Min Zhang John H.Adams Rays H.Y.Jiang | 2020 | Journal of Genetics and Genomics2020，47，9： | 1 |
| 3 | Loss of Notch signaling in skeletal stem cells enhances bone formation with aging显示文摘Skeletal stem and progenitor cells(SSPCs) perform bone maintenance and repair. With age, they produce fewer osteoblasts and more adipocytes leading to a loss of skeletal integrity. The molecular mechanisms that underlie this detrimental transformation are largely unknown. Single-cell RNA sequencing revealed that Notch signaling becomes elevated in SSPCs during aging. To examine the role of increased Notch activity, we deleted Nicastrin, an essential Notch pathway component, in SSPCs in vivo. Middle-aged conditional knockout mice displayed elevated SSPC osteo-lineage gene expression, increased trabecular bone mass, reduced bone marrow adiposity, and enhanced bone repair. Thus, Notch regulates SSPC cell fate decisions, and moderating Notch signaling ameliorates the skeletal aging phenotype, increasing bone mass even beyond that of young mice. Finally, we identified the transcription factor Ebf3 as a downstream mediator of Notch signaling in SSPCs that is dysregulated with aging, highlighting it as a promising therapeutic target to rejuvenate the aged skeleton. | Lindsey H.Remark Kevin Leclerc Malissa Ramsukh Ziyan Lin Sooyeon Lee Backialakshmi Dharmalingam Lauren Gillinov Vasudev V.Nayak Paulo El Parente Margaux Sambon Pablo J.Atria Mohamed A.E.Ali Lukasz Witek Alesha B.Castillo Christopher Y.Park Ralf H.Adams Aristotelis Tsirigos Sophie M.Morgani Philipp Leucht | 2023 | Bone Research2023，11，4： | 0 |
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