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Genome-wide identification of smad/foxh1 targets reveals a role for foxh1 in retinoic acid regulation and forebrain development (vol 14, pg 411, 2008)

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DEVELOPMENTAL CELL 2008年第4期14卷 633-633页

作者： Silvestri, Cristoforo Narimatsu, Masahiro von Both, Ingo Liu, Yongmei Tan, Nicholas B. J. Izzi, Luisa McCaffery, Peter Wrana, Jeffrey L. Attisano, Liliana Institute of Medical Science University of Toronto 160 College Street Toronto Ontario M5S 3E1 Canada Donnelly Centre for Cellular and Biomolecular Research University of Toronto 160 College Street Toronto Ontario M5S 3E1 Canada Program in Molecular Biology and Cancer Samuel Lunenfeld Research Institute Mount Sinai Hospital 600 University Avenue Toronto Ontario M5G 1X5 Canada Department of Biochemistry University of Toronto 160 College Street Toronto Ontario M5S 3E1 Canada Department of Medical Biophysics University of Toronto 160 College Street Toronto Ontario M5S 3E1 Canada Institute of Medical Sciences University of Aberdeen Foresterhill Aberdeen AB25 2ZD United Kingdom Department of Medical Genetics and Microbiology University of Toronto 160 College Street Toronto Ontario M5S 3E1 Canada

Foxh1, a Smad DNA-binding partner, mediates TGFβ-dependent gene expression during early development. Few Foxh1 targets are known. Here, we describe a genome-wide approach that we developed that couples systematic mapping of a functional Smad/Foxh1 enhancer (SFE) to Site Search, a program used to search annotated genomes for composite response elements. Ranking of SFEs that are positionally conserved across species yielded a set of genes enriched in Foxh1 targets. Analysis of top candidates, such as Hesx1 , Lgr4 , Lmo1 , Fgf8 , and members of the Aldh1a subfamily, revealed that Foxh1 initiates a transcriptional regulatory network within the developing anterior neuroectoderm. The Aldh1a family is required for retinoic acid (RA) synthesis, and, in Foxh1 mutants, expression of Aldh1a1 , - 2 , and - 3 and activation of a RA-responsive transgenic reporter is abolished in anterior structures. Integrated mapping of a developmental transcription factor network thus reveals a key role for Foxh1 in patterning and initiating RA signaling in the forebrain.

关键词： DEVBIO

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Developmental stage classification of Embryos using two-stream neural network with linear-chain conditional random field

arXiv

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arXiv 2021年

作者： Lukyanenko, Stanislav Jang, Won-Dong Wei, Donglai Struyven, Robbert Kim, Yoon Leahy, Brian Yang, Helen Rush, Alexander Ben-Yosef, Dalit Needleman, Daniel Pfister, Hanspeter Department of Informatics Technical University of Munich Germany School of Engineering and Applied Sciences Harvard University United States Department of Molecular and Cellular Biology Harvard University United States Graduate Program in Biophysics Harvard University United States University College London United Kingdom MIT United States Cornell University United States Center for Computational Biology Flatiron Institute United States Lis Maternity Hospital Tel-Aviv Sourasky Medical Center Israel Cell and Developmental Biology Tel-Aviv University Israel

The developmental process of embryos follows a monotonic order. An embryo can progressively cleave from one cell to multiple cells and finally transform to morula and blastocyst. For time-lapse videos of embryos, most existing developmental stage classification methods conduct per-frame predictions using an image frame at each time step. However, classification using only images suffers from overlapping between cells and imbalance between stages. Temporal information can be valuable in addressing this problem by capturing movements between neighboring frames. In this work, we propose a two-stream model for developmental stage classification. Unlike previous methods, our two-stream model accepts both temporal and image information. We develop a linear-chain conditional random field (CRF) on top of neural network features extracted from the temporal and image streams to make use of both modalities. The linear-chain CRF formulation enables tractable training of global sequential models over multiple frames while also making it possible to inject monotonic development order constraints into the learning process explicitly. We demonstrate our algorithm on two time-lapse embryo video datasets: i) mouse and ii) human embryo datasets. Our method achieves 98.1% and 80.6% for mouse and human embryo stage classification, respectively. Our approach will enable more profound clinical and biological studies and suggests a new direction for developmental stage classification by utilizing temporal information. Copyright © 2021, The Authors. All rights reserved.

关键词： Classification (of information)

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A 20 YEAR CLINICAL AND LABORATORY STUDY OF FAMILIAL B-CHRONIC LYMPHOCYTIC-LEUKEMIA IN A SINGLE KINDRED

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LEUKEMIA & LYMPHOMA 1991年第5-6期3卷 331-&页

作者： CAPORASO, NE WHITEHOUSE, J BERTIN, P AMOS, C PAPADOPOULOS, N MULLER, J WHANGPENG, J TUCKER, MA FLEISHER, TA MARTI, GE a Family Studies Section Epidemiology and Biostatistics Program NCI NIH 439E Executive Plaza North Bethesda Maryland USA. b Laboratory of Cellular and Molecular Biology Division of Biochemistry and Biophysics CBER FDA NIH Bdg 29 Rm 502 Bethesda Maryland USA. c Clinical Chemistry CPD CC NIH Bethesda Maryland USA. d Division of Virology CBER FDA Bethesda Maryland USA. e Cytogenetic Oncology Medicine Branch NCI Bethesda Maryland USA. f Immunology Service CPD CC NIH Bethesda Maryland USA.

Four siblings and a parent in a single kindred had documented blood and marrow lymphocytosis during the past 18 to 20 years consistent with chronic lymphocytic leukemia (CLL). Of the four siblings, one developed a spontaneous remission; one died secondary to subepiglotitis with sepsis; one died with prolymphocytoid transformation and one remains alive with splenomegalic CLL. Lymphadenopathy and splenomegaly were variable as was the clinical response to chemotherapy. Bone marrow morphology was initially nodular but progessed to diffuse patterns in both deceased siblings. Blood lymphocyte morphology was extremely variable as were cell doubling times and cytogenetic studies. ABO and HLA typing revealed no evidence of linkage. Immunophenotypic analysis of the B lymphocytes demonstrated a CD19 +, CD20-, CD5 +, Leu8-, Kappa + and a CD19 +, CD20 +, CD5 +, Leu8 +, Kappa + monoclonal lymphocytosis in two affected members. An unaffected sibling showed a CD4 lymphocytosis. VHV and VHII gene sequences were previously described in this kindred (PNAS 84: 8563, '87). We speculate that a CD5 B cell and CD4 T cell lymphocytosis may arise early in this disease followed by the development of a pleomorphic, monoclonal lymphocytosis. The subsequent oligomorphic, monoclonal lymphocytosis shows genotypic, immunophenotypic and some morphological heterogeneity consistent with ongoing differentiation. The longitudinal investigation of familial CLL offers a unique opportunity to study the sequence of events related to the natural history of B-CLL.

关键词： FAMILY STUDIES B-CLL LYMPHOCYTIC LEUKEMIA SINGLE KINDRED CLL

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Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates (vol 544, pg 245, 2017)

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NATURE 2024年第8017期630卷 E11-E11页

作者： Mall, Moritz Kareta, Michael S. Chanda, Soham Ahlenius, Henrik Perotti, Nicholas Zhou, Bo Grieder, Sarah D. Ge, Xuecai Drake, Sienna Ang, Cheen Euong Walker, Brandon M. Vierbuchen, Thomas Fuentes, Daniel R. Brennecke, Philip Nitta, Kazuhiro R. Jolma, Arttu Steinmetz, Lars M. Taipale, Jussi Suedhof, Thomas C. Wernig, Marius Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine Stanford University Stanford California USA Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute Stanford University Stanford California USA Department of Clinical Sciences Division of Neurology and Lund Stem Cell Center Lund University Lund Sweden Department of Developmental Biology Stanford University Stanford California USA Department of Genetics Stanford University Stanford California USA Genome Biology Unit European Molecular Biology Laboratory (EMBL) Heidelberg Germany Division of Functional Genomics and Systems Biology Department of Medical Biochemistry and Biophysics Karolinska Institutet Stockholm Sweden Genome Scale Biology Program University of Helsinki Helsinki Finland

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Structures of the HER2-HER3-NRG1 beta complex reveal a dynamic dimer interface (vol 600, pg 339, 2021)

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NATURE 2022年第7898期602卷 E26-E26页

作者： Diwanji, Devan Trenker, Raphael Thaker, Tarjani M. Wang, Feng Agard, David A. Verba, Kliment A. Jura, Natalia Cardiovascular Research Institute University of California San Francisco San Francisco CA USA Medical Scientist Training Program University of California San Francisco San Francisco CA USA Department of Chemistry and Biochemistry The University of Arizona Tucson AZ USA Department of Cellular and Molecular Pharmacology University of California San Francisco San Francisco CA USA Department of Biochemistry and Biophysics University of California San Francisco San Francisco CA USA Quantitative Biosciences Institute (QBI) University of California San Francisco San Francisco CA USA Department of Pharmaceutical Chemistry University of California San Francisco San Francisco CA USA

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Correction: Alzheimer risk gene product Pyk2 suppresses tau phosphorylation and phenotypic effects of tauopathy

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molecular neurodegeneration 2022年第1期17卷 56页

作者： A Harrison Brody Sarah Helena Nies Fulin Guan Levi M Smith Bandhan Mukherjee Santiago A Salazar Suho Lee Tu Kiet T Lam Stephen M Strittmatter Cellular Neuroscience Neurodegeneration and Repair Program Departments of Neurology and Neuroscience Yale School of Medicine New Haven CT USA. Graduate School of Cellular and Molecular Neuroscience University of Tübingen D-72074 Tübingen Germany. Department of Molecular Biophysics and Biochemistry Yale School of Medicine New Haven CT USA. Keck MS & Proteomics Resource Yale School of Medicine New Haven CT USA. Cellular Neuroscience Neurodegeneration and Repair Program Departments of Neurology and Neuroscience Yale School of Medicine New Haven CT USA. stephen.strittmatter@yale.edu.

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Evaluating Methods for the Prediction of Cell Type-Specific Enhancers in the Mammalian Cortex

SSRN

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SSRN 2024年

作者： Johansen, Nelson J. Kempynck, Niklas Zemke, Nathan R. Somasundaram, Saroja Winter, Seppe De Hooper, Marcus Dwivedi, Deepanjali Lohia, Ruchi Wehbe, Fabien Li, Bocheng Abaffyová, Darina Armand, Ethan J. Man, Julie De Eksi, Eren Can Hecker, Nikolai Hulselmans, Gert Konstantakos, Vasilis Mauduit, David Mich, John K. Partel, Gabriele Daigle, Tanya L. Levi, Boaz P. Zhang, Kai Tanaka, Yoshiaki Gillis, Jesse Ting, Jonathan T. Ben-Simon, Yoav Miller, Jeremy Ecker, Joseph R. Ren, Bing Aerts, Stein Lein, Ed S. Tasic, Bosiljka Bakken, Trygve E. Allen Institute for Brain Science SeattleWA98109 United States VIB Center for AI & Computational Biology VIB-KU Leuven Center for Brain and Disease Research KU Leuven Department of Human Genetics Leuven Belgium Center for Epigenomics Department of Cellular and Molecular Medicine University of California La Jolla San DiegoCA92093 United States Physiology Department Donnelly Centre for Cellular and Biomolecular Research University of Toronto TorontoON Canada Maisonneuve-Rosemont Hospital Research Centre University of Montreal MontrealQC Canada School of Life Sciences Westlake University Zhejiang Hangzhou China Bioinformatics and Systems Biology Program University of California La Jolla San DiegoCA92093 United States Westlake Laboratory of Life Sciences and Biomedicine Zhejiang Hangzhou China Department of Physiology and Biophysics University of Washington SeattleWA98195 United States Salk Institute for Biological Studies La Jolla CA92037 United States

Identifying cell type-specific enhancers in the brain is critical to building genetic tools for investigating the mammalian brain. Computational methods for functional enhancer prediction have been proposed and validated in the fruit fly and not yet the mammalian brain. We organized the "Brain Initiative Cell Census Network (BICCN) Challenge: Predicting Functional Cell Type-Specific Enhancers from Cross-Species Multi- Omics" to assess machine learning and feature-based methods designed to nominate enhancer DNA sequences to target cell types in the mouse cortex. Methods were evaluated based on in vivo validation data from hundreds of cortical cell type-specific enhancers that were previously packaged into individual AAV vectors and retro-orbitally injected into mice. We find that open chromatin was a key predictor of functional enhancers, and sequence models improved prediction of non-functional enhancers that can be deprioritized as opposed to pursued for in vivo testing. Sequence models also identified cell type-specific transcription factor codes that can guide designs of in silico enhancers. This community challenge establishes a benchmark for enhancer prioritization algorithms and reveals computational approaches and molecular information that are crucial for the identification of functional enhancers for mammalian cortical cell types. The results of this challenge bring us closer to understanding the complex gene regulatory landscape of the mammalian brain and help us design more efficient genetic tools and potential gene therapies for human neurological diseases. © 2024, The Authors. All rights reserved.

关键词： Mammals

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Correction to: An Easy-to-Fabricate Cell Stretcher Reveals Density-Dependent Mechanical Regulation of Collective Cell Movements in Epithelia

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cellular and molecular bioengineering 2021年第6期14卷 661-662页

作者： Kevin C Hart Joo Yong Sim Matthew A Hopcroft Daniel J Cohen Jiongyi Tan W James Nelson Beth L Pruitt Department of Biology Stanford University Stanford CA 94305 USA. IGM Biosciences Mountain View CA 94043 USA. Department of Mechanical Engineering Stanford University Stanford CA 94305 USA. Sookmyung Women's University Seoul 04310 Republic of Korea. Red Dog Research Santa Barbara CA 93109 USA. Department of Mechanical Engineering University of California 494 UCEN Rd Santa BarbaraSanta Barbara CA USA. Department of Mechanical and Aerospace Engineering Princeton University Princeton NJ 08544 USA. Department of Biophysics Stanford University Stanford CA 94305 USA. Department of Cellular and Molecular Pharmacology University of California San Francisco San Francisco CA 94143 USA. Biomolecular Science and Engineering Program University of California Santa Barbara Santa Barbara CA 93106 USA.

[This corrects the article DOI: 10.1007/s12195-021-000689-6.].

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Author Correction: Functional genomics data: privacy risk assessment and technological mitigation

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Nature reviews. Genetics 2022年第4期23卷 259页

作者： Gamze Gürsoy Tianxiao Li Susanna Liu Eric Ni Charlotte M Brannon Mark B Gerstein Computational Biology and Bioinformatics Program Yale University New Haven CT USA. Molecular Biophysics and Biochemistry Yale University New Haven CT USA. Molecular Cellular and Developmental Biology Yale University New Haven CT USA. Statistics and Data Science Yale University New Haven CT USA. Department of Biology Stanford University Stanford CA USA. Computational Biology and Bioinformatics Program Yale University New Haven CT USA. mark@***. Molecular Biophysics and Biochemistry Yale University New Haven CT USA. mark@***. Statistics and Data Science Yale University New Haven CT USA. mark@***. Computer Science Yale University New Haven CT USA. mark@***.

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AAA + ATPase Thorase inhibits mTOR signaling through the disassembly of the mTOR complex 1

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Nature Communications 2022年第1期13卷 1-18页

作者： Umanah, George K. E. Abalde-Atristain, Leire Khan, Mohammed Repon Mitra, Jaba Dar, Mohamad Aasif Chang, Melissa Tangella, Kavya McNamara, Amy Bennett, Samuel Chen, Rong Aggarwal, Vasudha Cortes, Marisol Worley, Paul F. Ha, Taekjip Dawson, Ted M. Dawson, Valina L. Neuroregeneration and Stem Cell Programs Institute for Cell Engineering Johns Hopkins University School of Medicine Baltimore 21205 MD United States Department of Neurology Johns Hopkins University School of Medicine Baltimore 21205 MD United States Cellular and Molecular Medicine Graduate Program Johns Hopkins University School of Medicine Baltimore 21205 MD United States Department of Materials Science and Engineering University of Illinois at Urbana-Champaign Urbana 61801 IL United States Department of Biophysics and Biophysical Chemistry Johns Hopkins University Baltimore 21205 MD United States Solomon H. Snyder Department of Neuroscience Johns Hopkins University School of Medicine Baltimore 21205 MD United States Departments of Biophysics and Biophysical Chemistry Biophysics and Biomedical Engineering JHU Howard Hughes Medical Institute Baltimore 21205 MD United States Department of Pharmacology and Molecular Sciences Johns Hopkins University School of Medicine Baltimore 21205 MD United States Department of Physiology Johns Hopkins University School of Medicine Baltimore 21205 MD United States Division of Neuroscience National Institute of Neurological Disorders and Stroke National Institutes of Health Bethesda MD United States Vollum Institute Oregon Health & Science University Portland 97239 OR United States

The mechanistic target of rapamycin (mTOR) signals through the mTOR complex 1 (mTORC1) and the mTOR complex 2 to maintain cellular and organismal homeostasis. Failure to finely tune mTOR activity results in metabolic dysregulation and disease. While there is substantial understanding of the molecular events leading mTORC1 activation at the lysosome, remarkably little is known about what terminates mTORC1 signaling. Here, we show that the AAA + ATPase Thorase directly binds mTOR, thereby orchestrating the disassembly and inactivation of mTORC1. Thorase disrupts the association of mTOR to Raptor at the mitochondria-lysosome interface and this action is sensitive to amino acids. Lack of Thorase causes accumulation of mTOR-Raptor complexes and altered mTORC1 disassembly/re-assembly dynamics upon changes in amino acid availability. The resulting excessive mTORC1 can be counteracted with rapamycin in vitro and in vivo. Collectively, we reveal Thorase as a key component of the mTOR pathway that disassembles and thus inhibits mTORC1. © 2022, The Author(s).

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