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Spliceosomal genes in the *** genome:a comparison with those in ***,***,*** and ***

Protein & Cell 2011年第5期2卷 395-409页

作者： Bing Yu Petra Fey Karen E.Kestin-Pilcher Alexei Fedorov Ashwin Prakash Rex L.Chisholm Jane Y.Wu Department of Molecular and Clinical Genetics Royal Prince Alfred Hospital and Sydney Medical School(Central)the University of SydneyNSW 2006Australia dictyBase Center for Genetic MedicineNorthwestern UniversityChicagoIL 60611USA Department of Neurology and Lurie Comprehensive Cancer Center Center for Genetic MedicineNorthwestern University Feinberg Medical SchoolChicagoIL 60611USA Department of Medicine and Program in Bioinformatics and Proteomics/Genomics The University of ToledoToledoOH 43614USA

Little is known about pre-mRNA splicing in Dictyostelium discoideum although its genome has been completely *** analysis suggests that pre-mRNA splicing plays an important role in *** gene expression as two thirds of its genes contain at least one *** curation of the genome to date has revealed 40 genes in *** with clear evidence of alternative splicing,supporting the existence of alternative splicing in this unicellular *** identified 160 candidate U2-type spliceosomal proteins and related factors in *** based on 264 known human genes involved in *** small ribonucleoproteins(snRNPs),PRP19 complex proteins and late-acting proteins are highly conserved in *** and throughout the *** non-snRNP and hnRNP families,*** orthologs are closer to those in ***,*** and *** than to their counterparts in *** splicing regulators,including SR proteins and CUGbinding proteins,were found in ***,but not in *** comprehensive catalog of spliceosomal proteins provides useful information for future studies of splicing in *** where the efficient genetic and biochemical manipulation will also further our general understanding of pre-mRNA splicing.

关键词： pre-mRNA splicing spliceosomal genes Dictyostelium discoideum comparative genomics splicing regulators

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The Alternative Splicing Mutation Database: A hub for investigations of alternative splicing using mutational evidence

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BMC Research Notes 2008年第1期1卷 1-7页

作者： Bechtel, Jason M. Rajesh, Preeti Ilikchyan, Irina Deng, Ying Mishra, Pankaj K. Wang, Qi Wu, Xiaochun Afonin, Kirill A. Grose, William E. Wang, Ye Khuder, Sadik Fedorov, Alexei Program in Bioinformatics and Proteomics/Genomics University of Toledo Health Science Campus Toledo OH 43614 United States Dept. of Medical Microbiology and Immunology University of Toledo Health Science Campus Toledo OH 43614 United States Dept. of Basic Pharmaceutical Sciences South Carolina College of Pharmacy University of South Carolina Columbia SC 29208 United States Department of Biological Sciences Bowling Green State University Bowling Green OH 43403 United States College of Engineering University of Toledo Toledo OH 43606 United States Dept. of Medicine University of Toledo Health Science Campus Toledo OH 43614 United States

Background. Some mutations in the internal regions of exons occur within splicing enhancers and silencers, influencing the pattern of alternative splicing in the corresponding genes. To understand how these sequence changes affect splicing, we created a database of these mutations. Findings. The Alternative Splicing Mutation Database (ASMD) serves as a repository for all exonic mutations not associated with splicing junctions that measurably change the pattern of alternative splicing. In this initial published release (version 1.2), only human sequences are present, but the ASMD will grow to include other organisms, (see Availability and requirements section for the ASMD web address). This relational database allows users to investigate connections between mutations and features of the surrounding sequences, including flanking sequences, RNA secondary structures and strengths of splice junctions. Splicing effects of the mutations are quantified by the relative presence of alternative mRNA isoforms with and without a given mutation. This measure is further categorized by the accuracy of the experimental methods employed. The database currently contains 170 mutations in 66 exons, yet these numbers increase regularly. We developed an algorithm to derive a table of oligonucleotide Splicing Potential (SP) values from the ASMD dataset. We present the SP concept and tools in detail in our corresponding article. Conclusion. The current data set demonstrates that mutations affecting splicing are located throughout exons and might be enriched within local RNA secondary structures. Exons from the ASMD have below average splicing junction strength scores, but the difference is small and is judged not to be significant. © 2008 Bechtel et al;licensee BioMed Central Ltd.

关键词： Alternative Splice Splice Effect Splice Junction Alternative Splice Effect mRNA Isoforms

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Calculation of splicing potential from the alternative splicing mutation database

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BMC Research Notes 2008年第1期1卷 1-6页

Background. The Alternative Splicing Mutation Database (ASMD) presents a collection of all known mutations inside human exons which affect splicing enhancers and silencers and cause changes in the alternative splicing pattern of the corresponding genes. Findings. An algorithm was developed to derive a Splicing Potential (SP) table from the ASMD information. This table characterizes the influence of each oligonucleotide on the splicing effectiveness of the exon containing it. If the SP value for an oligonucleotide is positive, it promotes exon retention, while negative SP values mean the sequence favors exon skipping. The merit of the SP approach is the ability to separate splicing signals from a wide range of sequence motifs enriched in exonic sequences that are attributed to protein-coding properties and/or translation efficiency. Due to its direct derivation from observed splice site selection, SP has an advantage over other computational approaches for predicting alternative splicing. Conclusion. We show that a vast majority of known exonic splicing enhancers have highly positive cumulative SP values, while known splicing silencers have core motifs with strongly negative cumulative SP values. Our approach allows for computation of the cumulative SP value of any sequence segment and, thus, gives researchers the ability to measure the possible contribution of any sequence to the pattern of splicing. © 2008 Bechtel et al;licensee BioMed Central Ltd.

关键词： Splice Enhancer Exonic Splice Enhancer Code Potential Constitutive Exon 14th Exon

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Dual-targeting compounds possessing enhanced anticancer activity via microtubule disruption and histone deacetylase inhibition

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European Journal of Medicinal Chemistry 2024年 265卷 116042页

作者： Tseng, Yu-Wei Yang, Tsung-Jung Hsu, Yuan-Ling Liu, Jyung-Hurng Tseng, Yin-Chen Hsu, Tse-Wei Lu, Yueh Pan, Szu-Hua Cheng, Ting-Jen Rachel Fang, Jim-Min Department of Chemistry National Taiwan University Taipei 106 Taiwan Graduate Institute of Medical Genomics and Proteomics College of Medicine National Taiwan University Taipei 100 Taiwan Graduate Institute of Genomics and Bioinformatics College of Life Sciences National Chung Hsing University Taichung 40227 Taiwan The Genomics Research Center Academia Sinica Taipei 115 Taiwan Doctoral Degree Program of Translational Medicine National Taiwan University Taipei 100 Taiwan Genome and Systems Biology Degree Program National Taiwan University and Academia Sinica Taipei 100 Taiwan

Dual-targeting anticancer agents 4–29 are designed by combining the structural features of purine-type microtubule-disrupting compounds and HDAC inhibitors. A library of the conjugate compounds connected by appropriate linkers was synthesized and found to possess HDACs inhibitory activity and render microtubule fragmentation by activating katanin, a microtubule-severing protein. Among various zinc-binding groups, hydroxamic acid shows the highest inhibitory activity of Class I HDACs, which was also reconfirmed by three-dimensional quantitative structure-activity relationship (3D-QSAR) pharmacophore prediction. The purine–hydroxamate conjugates exhibit enhanced cytotoxicity against MDA-MB231 breast cancer cells, H1975 lung cancer cells, and various clinical isolated non-small-cell lung cancer cells with different epidermal growth factor receptor (EGFR) status. Pyridyl substituents could be used to replace the C2 and N9 phenyl moieties in the purine-type scaffold, which can help to improve the solubility under physiological conditions, thus increasing cytotoxicity. In mice treated with the purine–hydroxamate conjugates, the tumor growth rate was significantly reduced without causing toxic effects. Our study demonstrates the potential of the dual-targeting purine–hydroxamate compounds for cancer monotherapy. © 2023 Elsevier Masson SAS

关键词： Breast cancer Histidine deacetylase Hydroxamate Katanin Lung cancer Microtubule Purine-type conjugate

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Response to mackay et Al

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Trends in biochemical sciences 2013年第9期38卷 423页

作者： Xiaodong Cheng Robert M Blumenthal Department of Biochemistry Emory University School of Medicine 1510 Clifton Road Atlanta GA 30322 USA Department of Medical Microbiology & Immunology and Program in Bioinformatics and Proteomics/Genomics The University of Toledo College of Medicine & Life Sciences Toledo OH 43614 USA

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Author Correction: π-HuB: the proteomic navigator of the human body

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Nature 2025年第8046期637卷 E22页

作者： Fuchu He Ruedi Aebersold Mark S Baker Xiuwu Bian Xiaochen Bo Daniel W Chan Cheng Chang Luonan Chen Xiangmei Chen Yu-Ju Chen Heping Cheng Ben C Collins Fernando Corrales Jürgen Cox Weinan E Jennifer E Van Eyk Jia Fan Pouya Faridi Daniel Figeys George Fu Gao Wen Gao Zu-Hua Gao Keisuke Goda Wilson Wen Bin Goh Dongfeng Gu Changjiang Guo Tiannan Guo Yuezhong He Albert J R Heck Henning Hermjakob Tony Hunter Narayanan Gopalakrishna Iyer Ying Jiang Connie R Jimenez Lokesh Joshi Neil L Kelleher Ming Li Yang Li Qingsong Lin Cui Hua Liu Fan Liu Guang-Hui Liu Yansheng Liu Zhihua Liu Teck Yew Low Ben Lu Matthias Mann Anming Meng Robert L Moritz Edouard Nice Guang Ning Gilbert S Omenn Christopher M Overall Giuseppe Palmisano Yaojin Peng Charles Pineau Terence Chuen Wai Poon Anthony W Purcell Jie Qiao Roger R Reddel Phillip J Robinson Paola Roncada Chris Sander Jiahao Sha Erwei Song Sanjeeva Srivastava Aihua Sun Siu Kwan Sze Chao Tang Liujun Tang Ruijun Tian Juan Antonio Vizcaíno Chanjuan Wang Chen Wang Xiaowen Wang Xinxing Wang Yan Wang Tobias Weiss Mathias Wilhelm Robert Winkler Bernd Wollscheid Limsoon Wong Linhai Xie Wei Xie Tao Xu Tianhao Xu Liying Yan Jing Yang Xiao Yang John Yates Tao Yun Qiwei Zhai Bing Zhang Hui Zhang Lihua Zhang Lingqiang Zhang Pingwen Zhang Yukui Zhang Yu Zi Zheng Qing Zhong Yunping Zhu State Key Laboratory of Medical Proteomics Beijing Proteome Research Center National Center for Protein Sciences (Beijing) Beijing Institute of Lifeomics Beijing China. hefc@***. International Academy of Phronesis Medicine (Guangdong) Guangdong China. hefc@***. Department of Biology Institute of Molecular Systems Biology ETH Zurich Zurich Switzerland. aebersold@imsb.biol.ethz.ch. Macquarie Medical School Macquarie University Sydney New South Wales Australia. Institute of Pathology and Southwest Cancer Center Southwest Hospital Third Military Medical University (Army Medical University) and Key Laboratory of Tumor Immunopathology Ministry of Education of China Chongqing China. Institute of Health Service and Transfusion Medicine Beijing China. Department of Pathology and The Sidney Kimmel Comprehensive Cancer Center Johns Hopkins University Baltimore MD USA. State Key Laboratory of Medical Proteomics Beijing Proteome Research Center National Center for Protein Sciences (Beijing) Beijing Institute of Lifeomics Beijing China. Key Laboratory of Systems Biology Center for Excellence in Molecular Cell Science Shanghai Institute of Biochemistry and Cell Biology Chinese Academy of Sciences Shanghai China. Department of Nephrology First Medical Center of Chinese PLA General Hospital Nephrology Institute of the Chinese People's Liberation Army State Key Laboratory of Kidney Diseases National Clinical Research Center for Kidney Diseases Beijing Key Laboratory of Kidney Disease Research Beijing China. Institute of Chemistry Academia Sinica Taipei China. National Biomedical Imaging Center State Key Laboratory of Membrane Biology Institute of Molecular Medicine Peking-Tsinghua Center for Life Sciences College of Future Technology Peking University Beijing China. School of Biological Sciences Queen's University of Belfast Belfast UK. Functional Proteomics Laboratory Centro Nacional de Biotecnología-CSIC Madrid Spain. Computational Systems Biochemistry Research Group Ma

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Characterization of primary Sjögren's syndrome in the Taiwan Han population through a genome-wide association study and polygenic risk score analysis

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Clinical Immunology 2024年 269卷 110381-110381页

作者： Liu, Ting-Yuan Lin, Min-Rou Lu, Hsing-Fang Chen, Yu-Chia Lin, Hui-Ju Chou, Wan-Hsuan Wei, Chun-Yu Palupi, Poppy Diah Liao, Chi-Chou Chang, Yen-Ting Chang, Wei-Chiao Tsai, Fuu-Jen Department of Medical Research China Medical University Hospital China Medical University Taichung 40447 Taiwan Department of Clinical Pharmacy School of Pharmacy Taipei Medical University Taipei 110 Taiwan Department of Ophthalmology Eye Center China Medical University Hospital Taichung 40447 Taiwan Master Program in Clinical Genomics and Proteomics School of Pharmacy Taipei Medical University Taipei 110 Taiwan Core Laboratory of Neoantigen Analysis for Personalized Cancer Vaccine Office of R&D Taipei Medical University Taipei 110 Taiwan Integrative Research Center in Critical Care Wanfang Hospital Taipei Medical University Taipei 116 Taiwan Department of Pharmacy Wan Fang Hospital Taipei Medical University Taipei 110 Taiwan Department of Pharmacology National Defense Medical Center Taipei 110 Taiwan Department of Medical Research China Medical University Hospital Taichung 40402 Taiwan School of Chinese Medicine China Medical University Taichung 40402 Taiwan Division of Pediatric Medical Genetics Children's Hospital of China Medical University Taichung 40447 Taiwan Department of Biotechnology and Bioinformatics Asia University Taichung 41354 Taiwan

Background: Sjögren's syndrome (SS) is an autoimmune disorder that primarily affects the exocrine glands, leading to dryness of mucous membranes and systemic manifestations. This study aimed to identify genetic markers associated with primary SS (pSS) in the Taiwan Han population through a hospital-based genome-wide association study (GWAS) and polygenic risk score (PRS) analysis, addressing the lack of genetic research. Results: This study included 11,390 patients diagnosed with pSS and 113,900 controls. GWAS identified one known locus and eight novel loci. Known HLA alleles, including HLA-DRB1*15:01 and HLA-DQA1*03:01, were successfully replicated in a consistent effect direction. PRS analysis revealed that several autoimmune diseases share similar genetic backgrounds with pSS, including rheumatoid arthritis and systemic lupus erythematosus. Conclusion: This study represents the largest cohort to date on the genetics of pSS in the Taiwan Han population. Our findings provide valuable insights into the pathogenesis of pSS and emphasize the comorbidities associated with it as an autoimmune disease. © 2024

关键词： Gene polymorphism Genome-wide association study (GWAS) Human leukocyte antigen (HLA) Phenome-wide association study (PheWAS) Polygenic risk score (PRS) Sjögren's syndrome

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A systems biology approach uncovers novel disease mechanisms in age-related macular degeneration

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Cell genomics 2023年第6期3卷 100302-100302页

作者： Orozco, Luz D. Owen, Leah A. Hofmann, Jeffrey Stockwell, Amy D. Tao, Jianhua Haller, Susan Mukundan, Vineeth T. Clarke, Christine Lund, Jessica Sridhar, Akshayalakshmi Mayba, Oleg Barr, Julie L. Zavala, Rylee A. Graves, Elijah C. Zhang, Charles Husami, Nadine Finley, Robert Au, Elizabeth Lillvis, John H. Farkas, Michael H. Shakoor, Akbar Sherva, Richard Kim, Ivana K. Kaminker, Joshua S. Townsend, Michael J. Farrer, Lindsay A. Yaspan, Brian L. Chen, Hsu-Hsin DeAngelis, Margaret M. Department of Bioinformatics and Computational Biology Genentech South San Francisco 94080 CA United States Department of Ophthalmology and Visual Sciences University of Utah School of Medicine The University of Utah Salt Lake City 84132 UT United States Department of Population Health Sciences University of Utah School of Medicine The University of Utah Salt Lake City 84132 UT United States Department of Obstetrics and Gynecology University of Utah School of Medicine The University of Utah Salt Lake City 84132 UT United States Department of Ophthalmology Ross Eye Institute Jacobs School of Medicine and Biomedical Sciences State University of New York University at Buffalo Buffalo 14203 NY United States Department of Pathology Genentech South San Francisco 94080 CA United States Department of Human Genetics Genentech South San Francisco 94080 CA United States Departments of Microchemistry Proteomics and Lipidomics Genentech South San Francisco 94080 CA United States Department of Human Pathobiology & OMNI Reverse Translation Genentech South San Francisco 94080 CA United States Neuroscience Graduate Program Jacobs School of Medicine and Biomedical Sciences State University of New York University at Buffalo Buffalo 14203 NY United States Department of Biochemistry Jacobs School of Medicine and Biomedical Sciences State University of New York University at Buffalo Buffalo 14203 NY United States Veterans Administration Western New York Healthcare System Buffalo 14212 NY United States Department of Medicine Biomedical Genetics Boston University School of Medicine Boston 02118 MA United States Retina Service Massachusetts Eye & Ear Department of Ophthalmology Harvard Medical School Boston 02114 MA United States Genetics Genomics and Bioinformatics Graduate Program Jacobs School of Medicine and Biomedical Sciences State University of New York University at Buffalo Buffalo 14203 NY United States

Age-related macular degeneration (AMD) is a leading cause of blindness, affecting 200 million people worldwide. To identify genes that could be targeted for treatment, we created a molecular atlas at different stages of AMD. Our resource is comprised of RNA sequencing (RNA-seq) and DNA methylation microarrays from bulk macular retinal pigment epithelium (RPE)/choroid of clinically phenotyped normal and AMD donor eyes (n = 85), single-nucleus RNA-seq (164,399 cells), and single-nucleus assay for transposase-accessible chromatin (ATAC)-seq (125,822 cells) from the retina, RPE, and choroid of 6 AMD and 7 control donors. We identified 23 genome-wide significant loci differentially methylated in AMD, over 1,000 differentially expressed genes across different disease stages, and an AMD Müller state distinct from normal or gliosis. Chromatin accessibility peaks in genome-wide association study (GWAS) loci revealed putative causal genes for AMD, including HTRA1 and C6orf223. Our systems biology approach uncovered molecular mechanisms underlying AMD, including regulators of WNT signaling, FRZB and TLE2, as mechanistic players in disease. © 2023 The Authors

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γ-Linolenic acid in maternal milk drives cardiac metabolic maturation (vol 618, pg 365, 2023)

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NATURE 2023年第7968期619卷 E24-E24页

作者： Paredes, Ana Justo-Mendez, Raquel Jimenez-Blasco, Daniel Nunez, Vanessa Calero, Irene Villalba-Orero, Maria Alegre-Marti, Andrea Fischer, Thierry Gradillas, Ana Sant'Anna, Viviane Aparecida Rodrigues Were, Felipe Huang, Zhiqiang Hernansanz-Agustin, Pablo Contreras, Carmen Martinez, Fernando Camafeita, Emilio Vazquez, Jesus Ruiz-Cabello, Jesus Area-Gomez, Estela Sanchez-Cabo, Fatima Treuter, Eckardt Bolanos, Juan Pedro Estebanez-Perpina, Eva Ruperez, Francisco Javier Barbas, Coral Enriquez, Jose Antonio Ricote, Mercedes Cardiovascular Regeneration Program Centro Nacional de Investigaciones Cardiovasculares (CNIC) Madrid Spain Departamento de Medicina y Cirugía Animal Universidad Complutense de Madrid (UCM) Madrid Spain CIBER de Fragilidad y Envejecimiento Saludable (CIBERFES) Madrid Spain Institute of Functional Biology and Genomics (IBFG) University of Salamanca CSIC Salamanca Spain Institute for Biomedical Research of Salamanca (IBSAL) Salamanca Spain Department of Biochemistry and Molecular Biomedicine Institute of Biomedicine (IBUB) of the University of Barcelona (UB) Barcelona Spain Department of Immunology and Oncology Centro Nacional de Biotecnología-Consejo Superior de Investigaciones Científicas (CNB/CSIC) Campus Universidad Autónoma de Madrid (UAM) Madrid Spain Centro de Metabolómica y Bioanálisis (CEMBIO) Facultad de Farmacia Universidad San Pablo-CEU CEU Universities Madrid Spain Bioinformatics Unit Centro Nacional de Investigaciones Cardiovasculares (CNIC) Madrid Spain CIBER de Enfermedades Cardiovasculares (CIBERCV) Madrid Spain Department of Biosciences and Nutrition Karolinska Institutet Huddinge Sweden Proteomics Unit Centro Nacional de Investigaciones Cardiovasculares (CNIC) Madrid Spain CIC biomaGUNE Basque Research and Technology Alliance (BRTA) San Sebastian Spain Ikerbasque Basque Foundation for Science Bilbao Spain CIBER de Enfermedades Respiratorias (CIBERES) Madrid Spain Departamento de Ciencias Farmacéuticas Facultad de Farmacia Universidad Complutense Madrid (UCM) Madrid Spain Departament of Cellular and Molecular Biology Centro de Investigaciones Biológicas Margarita Salas-CSIC Madrid Spain Department of Neurology Columbia University Medical Campus New York NY USA

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JS08.6.A A connectivity signature for glioblastoma

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Neuro-Oncology 2022年第SUPPLEMENT_2期24卷 ii8-ii9页

作者： Hoffmann, D C Hai, L Wagener, R Mandelbaum, H Xie, R Hausmann, D Dominguez Azorín, D Weil, S Sievers, P Cebulla, G Ito, J Warnken, U Venkataramani, V Ernst, K Reibold, D Will, R Suvà, M L Herold-Mende, C Sahm, F Winkler, F Schlesner, M Wick, W Kessler, T Clinical Cooperation Unit Neurooncology German Cancer Consortium (DKTK) German Cancer Research Center (DKFZ) Heidelberg Germany Department of Neurology and Neurooncology Program National Center for Tumor Diseases Heidelberg University Hospital Heidelberg Germany Faculty of Biosciences Heidelberg University Heidelberg Germany Bioinformatics and Omics Data Analytics DKFZ Heidelberg Germany Department of Neuropathology Institute of Pathology University Hospital Heidelberg Heidelberg Germany Clinical Cooperation Unit Neuropathology DKTK DKFZ Heidelberg Germany Department of Neuroanatomy Institute for Anatomy and Cell Biology Heidelberg University Heidelberg Germany Hopp Children's Cancer Center at the NCT Heidelberg (KiTZ) Heidelberg Germany Division of Pediatric Neurooncology DKTK DKFZ Heidelberg Germany Genomics and Proteomics Core Facility DKTK DKFZ Heidelberg Germany Broad Institute of Harvard and MIT Cambridge MA United States Department of Pathology and Center for Cancer Research Massachusetts General Hospital and Harvard Medical School Boston MA United States Department of Neurosurgery Heidelberg University Hospital Heidelberg Germany Biomedical Informatics Data Mining and Data Analytics Faculty of Applied Computer Science and Medical Faculty University of Augsburg Augsburg Germany

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