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Author Correction: The Rho GTPase Rnd1 suppresses mammary tumorigenesis and EMT by restraining Ras-MAPK signalling

Nature cell biology 2019年第4期21卷 534页

作者： Tomoyo Okada Surajit Sinha Ilaria Esposito Gaia Schiavon Miguel A López-Lago Wenjing Su Christine A Pratilas Cristina Abele Jonathan M Hernandez Masahiro Ohara Morihito Okada Agnes Viale Adriana Heguy Nicholas D Socci Anna Sapino Venkatraman E Seshan Stephen Long Giorgio Inghirami Neal Rosen Filippo G Giancotti Cell Biology Program Sloan-Kettering Institute for Cancer Research Memorial Sloan-Kettering Cancer Center New York New York 10065 USA. Department of Surgery Memorial Sloan-Kettering Cancer Center New York 10065 USA. Breast Unit Royal Marsden Hospital London SW3 6JJ UK. Department of Surgery and Center for Cell Engineering Memorial Sloan-Kettering Cancer Center New York 10065 USA. Molecular Pharmacology and Chemistry Program Sloan-Kettering Institute for Cancer Research Memorial Sloan-Kettering Cancer Center New York New York 10065 USA. Department of Pediatrics Memorial Hospital Memorial Sloan-Kettering Cancer Center New York New York 10065 USA. The Sidney Kimmel Comprehensive Cancer Center Johns Hopkins University School of Medicine Baltimore Maryland 21287 USA. Department of Biomedical Sciences and Human Oncology Center of Experimental Medicine and Research University of Torino Torino 10126 Italy. Department of Surgery Memorial Hospital Memorial Sloan-Kettering Cancer Center New York New York 10065 USA. Department of Surgical Oncology Research Institute for Radiation Biology and Medicine Graduate School of Biomedical Sciences Hiroshima University Hiroshima 734-8551 Japan. Genomics Core Facility Memorial Sloan-Kettering Cancer Center New York New York 10065 USA. Geoffrey Beene Translational Oncology Core Facility Memorial Sloan-Kettering Cancer Center New York New York 10065 USA. Department of Pathology Office for Collaborative Science New York University New York 10016 USA. Bioinformatics Core Facility Memorial Sloan-Kettering Cancer Center New York New York 10065 USA. Department of Medical Sciences Center of Experimental Medicine and Research University of Torino Torino 10126 Italy. Department of Epidemiology and Biostatistics Memorial Hospital Memorial Sloan-Kettering Cancer Center New York New York 10065 USA. Structural Biology Program Sloan-Kettering Institute for Cancer Research Memorial Sloan-Kettering Cancer Center New Y

In the version of this Article originally published the same blot was inadvertently presented as both p-Rb and Cyclin A in Fig. 2a. This blot corresponds to the p-Rb panel, as can be seen in the unprocessed version of these blots in Supplementary Fig. 9. The corrected version of the panel is shown below, together with a completely uncropped image of both blots. In addition, in the 'Viral transduction' section of the Methods, the pLKO.1 plasmids encoding short hairpin RNAs targeting human Rnd1 were incorrectly listed as clones TRCN0000018338 and TRCN0000039977. The correct clone numbers are TRCN0000047434 and TRCN0000047435.

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Monitoring microbial responses to ocean deoxygenation in a model oxygen minimum zone

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Scientific Data 2017年第1期4卷 1-3页

作者： Hallam, Steven J. Torres-Beltrán, Mónica Hawley, Alyse K. Department of Microbiology and Immunology University of British Columbia Vancouver V6T 1Z3 BC Canada Peter Wall Institute for Advanced Studies University of British Columbia Vancouver V6T 1Z2 BC Canada Genome Science and Technology Program University of British Columbia Vancouver V6T 1Z4 BC Canada Graduate Program in Bioinformatics University of British Columbia Vancouver V6T 1Z4 BC Canada ECOSCOPE Training Program University of British Columbia Vancouver V6T 1Z4 BC Canada

Today in Scientific Data, two compendia of geochemical and multi-omic sequence information (DNA, RNA, protein) generated over almost a decade of time series monitoring in a seasonally anoxic coastal marine setting are presented to the scientific community. These data descriptors introduce a model ecosystem for the study of microbial responses to ocean deoxygenation, a phenotype that is currently expanding due to climate change. Public access to this time series information is intended to promote scientific collaborations and the generation of new hypotheses relevant to microbial ecology, biogeochemistry and global change issues. © The Author(s) 2017.

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Public Good Diffusion Limits Microbial Mutualism

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Physical Review Letters 2015年第16期114卷 168102-168102页

作者： Rajita Menon Kirill S. Korolev Department of Physics and Graduate Program in Bioinformatics Boston University Boston Massachusetts 02215 USA

Standard game theory cannot describe microbial interactions mediated by diffusible molecules. Nevertheless, we show that one can still model microbial dynamics using game theory with parameters renormalized by diffusion. Contrary to expectations, greater sharing of metabolites reduces the strength of cooperation and leads to species extinction via a nonequilibrium phase transition. We report analytic results for the critical diffusivity and the length scale of species intermixing. Species producing slower public good is favored by selection when fitness saturates with nutrient concentration.

关键词： Game theory

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Systems biology applications to study mechanisms of human immunodeficiency virus latency and reactivation

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World Journal of Clinical Infectious Diseases 2016年第2期6卷 6-21页

作者： Cory H White Bastiaan Moesker Angela Ciuffi Nadejda Beliakova-Bethell Graduate Program in Bioinformatics and Systems Biology University of California San Diego San Diego VA Medical Center and Veterans Medical Research Foundation Clinical and Experimental Sciences Faculty of Medicine University of Southampton Institute of Microbiology University Hospital of Lausanne (CHUV) and University of Lausanne Department of Medicine Univer-sity of California San Diego

Eradication of human immunodeficiency virus(HIV) in infected individuals is currently not possible because of the presence of the persistent cellular reservoir of latent infection. The identification of HIV latency biomarkers and a better understanding of the molecular mechanisms contributing to regulation of HIV expression might provide essential tools to eliminate these latently infected cells. This review aims at summarizing gene expression profiling and systems biology applications to studies of HIV latency and eradication. Studies comparing gene expression in latently infected and uninfected cells identify candidate latency biomarkers and novel mechanisms of latency control. Studies that profiled gene expression changes induced by existing latency reversing agents(LRAs) highlight uniting themes driving HIV reactivation and novel mechanisms that contribute to regulation of HIV expression by different LRAs. Among the reviewed gene expression studies, the common approaches included identification of differentially expressed genes and gene functional category assessment. Integration of transcriptomic data with other biological data types is presently scarce, and the field would benefit from increased adoption of these methods in future studies. In addition, designing prospective studies that use the same methods of data acquisition and statistical analyses will facilitate a more reliableidentification of latency biomarkers using different model systems and the comparison of the effects of different LRAs on host factors with a role in HIV reactivation. The results from such studies would have the potential to significantly impact the process by which candidate drugs are selected and combined for future evaluations and advancement to clinical trials.

关键词： Gene expression Microarrays RNA-Seq Systems biology Human immunodeficiency virus Viral latency Disease eradication Biomarkers Molecular mechanisms Latency reversing agents

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Evolution Arrests Invasions of Cooperative Populations

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Physical Review Letters 2015年第20期115卷 208104-208104页

作者： Kirill S. Korolev Department of Physics and Graduate Program in Bioinformatics Boston University Boston Massachusetts 02215 USA.

Population expansions trigger many biomedical and ecological transitions, from tumor growth to invasions of non-native species. Although population spreading often selects for more invasive phenotypes, we show that this outcome is far from inevitable. In cooperative populations, mutations reducing dispersal have a competitive advantage. Such mutations then steadily accumulate at the expansion front, bringing invasion to a halt. Our findings are a rare example of evolution driving the population into an unfavorable state, and they could lead to new strategies to combat unwelcome invaders.

关键词： Evolutionary dynamics Mutation

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Rejection of aliases for a direct sampling mixer with complex poles

IEEJ Transactions on Electronics, Information and Systems

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IEEJ Transactions on Electronics, Information and Systems 2016年第1期136卷 60-67页

作者： Imai, Hiroyuki Wada, Kazuyuki Electrical Engineering Program Graduate School of Science and Technology Meiji University 1-1-1 Higashi-Mita Tama-ku Kawasaki214-8571 Japan Department of Electronics and Bioinformatics School of Science and Technology Meiji University 1-1-1 Higashi-Mita Tama-ku Kawasaki214-8571 Japan

This paper proposes the design scheme of direct sampling mixer (DSM) by which unallowable amplitude characteristics due to aliases spreading over relatively broad band is suppressed. It is pointed out that the periodic frequency characteristic of a stage processing decimated signal causes decrease of attenuation in the stopband of the DSM, and an IIR section with a low decimation rate is employed as the first stage. A DSM the amplitude characteristic of which falls into the spectrum mask for IEEE 802.11 is designed as an example. Simulation results show that the designed DSM satisfies specification widely in not only the passband but also the stopband. It is confirmed that gradual decimation approach or use of a non-decimated section for the first stage is effective. © 2016 The Institute of Electrical Engineers of Japan.

关键词： Bandpass filters

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Corrigendum to "Plasma metabolomics in adults with cystic fibrosis during a pulmonary exacerbation: A pilot randomized study of high-dose vitamin D3 administration" [Metabolism vol. 70, May 2017, pages 31-41]

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Metabolism: clinical and experimental 2017年 74卷 41-42页

作者： Jessica A Alvarez Elizabeth Y Chong Douglas I Walker Joshua D Chandler Ellen S Michalski Ruth E Grossmann Karan Uppal Shuzhao Li Jennifer K Frediani Rabindra Tirouvanziam ViLinh T Tran Vin Tangpricha Dean P Jones Thomas R Ziegler Division of Endocrinology Metabolism & Lipids Department of Medicine Emory University School of Medicine Atlanta GA USA Center for Cystic Fibrosis and Airways Disease Research Children's Healthcare of Atlanta Atlanta GA USA. Electronic address: jessica.alvarez@emory.edu. Department of Biostatistics and Bioinformatics Rollins School of Public Health Emory University Atlanta GA USA. Division of Pulmonary Allergy Critical Care and Sleep Medicine Department of Medicine Emory University School of Medicine Atlanta GA USA. Center for Cystic Fibrosis and Airways Disease Research Children's Healthcare of Atlanta Atlanta GA USA Division of Pulmonary Allergy Critical Care and Sleep Medicine Department of Medicine Emory University School of Medicine Atlanta GA USA. Nutrition and Health Sciences Graduate Program Laney Graduate School Emory University Atlanta GA USA. College of Nursing The University of Iowa Ames IA USA. Division of Pulmonary Allergy & Immunology Cystic Fibrosis and Sleep Department of Pediatrics Emory University School of Medicine Atlanta GA USA. Center for Cystic Fibrosis and Airways Disease Research Children's Healthcare of Atlanta Atlanta GA USA Section of Endocrinology Atlanta Veterans Affairs Medical Center Atlanta GA USA.

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Random close packing in protein cores

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Physical Review E 2016年第3期93卷 032415-032415页

作者： Jennifer C. Gaines W. Wendell Smith Lynne Regan Corey S. O'Hern Program in Computational Biology and Bioinformatics Yale University New Haven Connecticut 06520 USA Integrated Graduate Program in Physical and Engineering Biology (IGPPEB) Yale University New Haven Connecticut 06520 USA Department of Physics Yale University New Haven Connecticut 06520 USA Department of Molecular Biophysics & Biochemistry Yale University New Haven Connecticut 06520 USA Department of Chemistry Yale University New Haven Connecticut 06520 USA Department of Mechanical Engineering & Materials Science Yale University New Haven Connecticut 06520 USA Department of Applied Physics Yale University New Haven Connecticut 06520 USA

Shortly after the determination of the first protein x-ray crystal structures, researchers analyzed their cores and reported packing fractions ϕ≈0.75, a value that is similar to close packing of equal-sized spheres. A limitation of these analyses was the use of extended atom models, rather than the more physically accurate explicit hydrogen model. The validity of the explicit hydrogen model was proved in our previous studies by its ability to predict the side chain dihedral angle distributions observed in proteins. In contrast, the extended atom model is not able to recapitulate the side chain dihedral angle distributions, and gives rise to large atomic clashes at side chain dihedral angle combinations that are highly probable in protein crystal structures. Here, we employ the explicit hydrogen model to calculate the packing fraction of the cores of over 200 high-resolution protein structures. We find that these protein cores have ϕ≈0.56, which is similar to results obtained from simulations of random packings of individual amino acids. This result provides a deeper understanding of the physical basis of protein structure that will enable predictions of the effects of amino acid mutations to protein cores and interfaces of known structure.

关键词： Protein structure Proteins

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Comprehensive Functional Characterization of Germline ETV6 Variants Associated with Inherited Predisposition to Acute Lymphoblastic Leukemia in Children

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BLOOD 2016年第22期128卷 1085-1085页

作者： Nishii, Rina Baskin, Rebekah Moriyama, Takaya Hoshitsuki, Keito Metzger, Monika L. Wu, Gang Devidas, Meenakshi Yang, Wenjian Tedrick, Paige Quinn, Emily Gastier-Foster, Julie M. Raetz, Elizabeth Larsen, Eric Martin, Paul L. Bowman, W. Paul Winick, Naomi Takagi, Masatoshi Pui, Ching-Hon Evans, William E. Zhang, Jinghui Relling, Mary V. Hunger, Stephen P. Mullighan, Charles Loh, Mignon L. Nichols, Kim E. Yang, Jun J. Hematological Malignancies Program and Department of Pharmaceutical Sciences St. Jude Children's Research Hospital Memphis TN Department of Pediatrics and Developmental Biology Tokyo Medical and Dental University Graduate School of Medicine Tokyo Japan Department of Oncology St. Jude Children's Research Hospital Memphis TN School of Pharmacy University of Pittsburgh Pittsburgh PA Department of Computational Biology St. Jude Children's Research Hospital Memphis TN Department of Biostatistics College of Medicine Public Health and Health Professions University of Florida Gainesville FL Department of Pathology and Laboratory Medicine Nationwide Children's Hospital Columbus OH Huntsman Cancer Institute University of Utah Salt Lake City UT Maine Children's Cancer Program Scarborough ME Department of Pediatrics Duke University Durham NC Cook Children's Medical Center Fort Worth TX Pediatric Hematology Oncology University of Texas Southwestern Medical Center Dallas TX Oncology St. Jude Children's Research Hospital Memphis TN Department of Computational Biology and Bioinformatics St. Jude Children's Research Hospital Memphis TN

There is increasing evidence for inherited susceptibility to acute lymphoblastic leukemia (ALL) in children. Both common and rare germline genetic variants can significantly influence the risk of developing ALL, often in an age- and/or leukemia subtype-dependent manner (e.g., ARID5B , IKZF1 , GATA3 , PIP4K2A , PAX5, and TP53 ). Recently, we and others reported a novel genetic syndrome characterized by damaging germline ETV6 mutations that co-segregate with hereditary thrombocytopenia and increased propensity for hematologic malignancies (especially ALL). Sequencing 4,405 childhood ALL cases, we subsequently identified 30 germline coding ETV6 variants that were potentially responsible for disease predisposition in 35 patients (Lancet Oncol 2015). These findings unequivocally point to ETV6 as a critical ALL risk gene; however, the exact functional consequences of the ALL-related ETV6 variants are largely unknown and the mechanism by which they contribute to leukemogenesis is unclear. To this end, we first systematically evaluated these 30 ETV6 risk variants for their transcriptional repressor activity, ability to bind to target DNA sequences, localize to the nucleus, and also to homo-dimerize. Using PF4 and MMP3 promoter-driven luciferase transcription in HEK293T cells as the model system, we showed that 18 of these 30 ETV6 variants had loss of transcriptional repression activity (median of 53.2% of wildtype ETV6 activity [range 7.1% to 83.9%]). These include 4 of the 5 frameshift variants, all 4 nonsense variants, and also 10 of 11 missense variants in the ETS/DNA binding domain. None of the missense variants outside the ETS domain had significant effects on transcriptional repression function, and surprisingly the E44fs variant showed enhanced activity. Co-expression of wildtype and each of the 18 loss-of-function variants consistently impaired the normal repressor activity of wildtype ETV6, indicating dominant-negative effects. In cells expressing both wildtype and

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Proceedings of the 16th Annual UT-KBRIN bioinformatics Summit 2016: bioinformatics

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BMC bioinformatics 2017年第9期18卷 1-9页

作者： Eric C. Rouchka Juw Won Park Julia H. Chariker David A. Tieri Shreedharkumar Rajurkar Vikas Singh Nishchal K. Verma Yan Cui Mark Farman Bradford Condon Jolanta Jaromczyk Neil Moore Jerzy Jaromczyk Daniel Harris Patrick Calie Eun Kyong Shin Robert L. Davis Arash Shaban-Nejad Joshua M. Mitchell Hunter N. B. Moseley Robert M. Flight Qing Jun Wang Richard M. Higashi Teresa W-M Fan Andrew N. Lane Liangqun Lu Bernie J Daigle Jr. Xi Chen Andrey Smelter Jerzy W. Jaromczyk Bailey K. Phan Nathaniel J. Serpico Ethan G. Toney Li Chen Caroline E. Melton Jennifer R. Mandel Bernie J. Daigle Jr. Hao Chen Kazi I. Zaman Ramin Homayouni Patrick J. Trainor Andrew P. DeFilippis Samantha M. Carlisle Shesh N. Rai Department of Computer Engineering and Computer Science University of Louisville Duthie Center for Engineering Louisville KY 40292 USA Kentucky Biomedical Research Infrastructure (KBRIN) Bioinformatics Core 522 East Gray Street Louisville KY 40292 USA Department of Psychological and Brain Sciences University of Louisville Louisville KY 40292 USA Department of Anatomical Sciences and Neurobiology University of Louisville Louisville KY 40292 USA Department of Electrical Engineering IIT Kanpur India Department of Microbiology Immunology and Biochemistry University of Tennessee Health Science Center Memphis TN 38103 USA Center for Integrative and Translational Genomics University of Tennessee Health Science Center Memphis TN 38103 USA Department of Plant Pathology University of Kentucky Lexington KY 40546 USA UK Healthcare Genomics University of Kentucky Lexington KY 40536 USA Department of Entomology & Plant Pathology University of Tennessee Knoxville TN 37996 USA Department of Forestry University of Kentucky Lexington KY 40506 USA Department of Computer Science University of Kentucky Lexington KY 40506 USA Department of Computer Science University of Kentucky Lexington KY 40508 USA Department of Biological Sciences Eastern Kentucky University Richmond KY 40475 USA University of Tennessee Health Science Center – Oak-Ridge National Lab (UTHSC-ORNL) Center for Biomedical Informatics Department of Pediatrics Memphis TN 38103 USA Department of Molecular & Cellular Biochemistry University of Kentucky Lexington KY 40536 USA Markey Cancer Center University of Kentucky Lexington KY 40536 USA Center for Environmental and Systems Biochemistry University of Kentucky Lexington KY 40536 USA Institute for Biomedical Informatics University of Kentucky Lexington KY 40536 USA Department of Molecular and Cellular Biochemistry University of Kentucky Lexington KY 40536 USA Department of Statistics University of Kentucky Louisville KY

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