Institution
Laboratory of Molecular Biology
Facility•Cambridge, Cambridgeshire, United Kingdom•
About: Laboratory of Molecular Biology is a facility organization based out in Cambridge, Cambridgeshire, United Kingdom. It is known for research contribution in the topics: Gene & RNA. The organization has 19395 authors who have published 24236 publications receiving 2101480 citations.
Topics: Gene, RNA, DNA, Population, Receptor
Papers published on a yearly basis
Papers
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Broad Institute1, Howard Hughes Medical Institute2, Massachusetts Institute of Technology3, Wellcome Trust Sanger Institute4, European Bioinformatics Institute5, University of Cambridge6, Harvard University7, Weizmann Institute of Science8, University of Zurich9, Laboratory of Molecular Biology10, Utrecht University11, École Polytechnique Fédérale de Lausanne12, University of Pennsylvania13, Heidelberg University14, German Cancer Research Center15, Ludwig Maximilian University of Munich16, John Radcliffe Hospital17, Newcastle University18, Stanford University19, University of Oxford20, University of California, San Francisco21, Allen Institute for Brain Science22, Karolinska Institutet23, Royal Institute of Technology24, Icahn School of Medicine at Mount Sinai25, University of Cape Town26, University Medical Center Groningen27, Radboud University Nijmegen28, Kettering University29, University of Edinburgh30, Babraham Institute31, New York University32, Netherlands Cancer Institute33, Ragon Institute of MGH, MIT and Harvard34, University of Texas Health Science Center at Houston35, Technische Universität München36, Technical University of Denmark37, University of California, Berkeley38, King's College London39, California Institute of Technology40
TL;DR: An open comprehensive reference map of the molecular state of cells in healthy human tissues would propel the systematic study of physiological states, developmental trajectories, regulatory circuitry and interactions of cells, and also provide a framework for understanding cellular dysregulation in human disease.
Abstract: The recent advent of methods for high-throughput single-cell molecular profiling has catalyzed a growing sense in the scientific community that the time is ripe to complete the 150-year-old effort to identify all cell types in the human body. The Human Cell Atlas Project is an international collaborative effort that aims to define all human cell types in terms of distinctive molecular profiles (such as gene expression profiles) and to connect this information with classical cellular descriptions (such as location and morphology). An open comprehensive reference map of the molecular state of cells in healthy human tissues would propel the systematic study of physiological states, developmental trajectories, regulatory circuitry and interactions of cells, and also provide a framework for understanding cellular dysregulation in human disease. Here we describe the idea, its potential utility, early proofs-of-concept, and some design considerations for the Human Cell Atlas, including a commitment to open data, code, and community.
1,391 citations
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TL;DR: It is shown that a large binding site for a protein antigen (lysozyme) can also be transplanted from mouse to human heavy chain and facilitated by an induced-fit mechanism.
Abstract: The production of therapeutic human monoclonal antibodies by hybridoma technology has proved difficult, and this has prompted the "humanizing" of mouse monoclonal antibodies by recombinant DNA techniques. It was shown previously that the binding site for a small hapten could be grafted from the heavy-chain variable domain of a mouse antibody to that of a human myeloma protein by transplanting the hypervariable loops. It is now shown that a large binding site for a protein antigen (lysozyme) can also be transplanted from mouse to human heavy chain. The success of such constructions may be facilitated by an induced-fit mechanism.
1,390 citations
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TL;DR: Evidence is reported that the syndecan heparan sulphate proteoglycans and their cytoplasmic adaptor syntenin control the formation of exosomes, indicating a key role for syndecans–syntenin–ALIX in membrane transport and signalling processes.
Abstract: The biogenesis of exosomes, small secreted vesicles involved in signalling processes, remains incompletely understood. Here, we report evidence that the syndecan heparan sulphate proteoglycans and their cytoplasmic adaptor syntenin control the formation of exosomes. Syntenin interacts directly with ALIX through LYPX(n)L motifs, similarly to retroviral proteins, and supports the intraluminal budding of endosomal membranes. Syntenin exosomes depend on the availability of heparan sulphate, syndecans, ALIX and ESCRTs, and impact on the trafficking and confinement of FGF signals. This study identifies a key role for syndecan-syntenin-ALIX in membrane transport and signalling processes.
1,390 citations
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TL;DR: Current understanding of the regulation of circRNA biogenesis is highlighted, including both the competition between splicing and back-splicing and the previously under-appreciated alternative circularization.
Abstract: Unlike linear RNAs terminated with 5′ caps and 3′ tails, circular RNAs are characterized by covalently closed loop structures with neither 5′ to 3′ polarity nor polyadenylated tail. This intrinsic characteristic has led to the general under-estimation of the existence of circular RNAs in previous polyadenylated transcriptome analyses. With the advent of specific biochemical and computational approaches, a large number of circular RNAs from back-spliced exons (circRNAs) have been identified in various cell lines and across different species. Recent studies have uncovered that back-splicing requires canonical spliceosomal machinery and can be facilitated by both complementary sequences and specific protein factors. In this review, we highlight our current understanding of the regulation of circRNA biogenesis, including both the competition between splicing and back-splicing and the previously under-appreciated alternative circularization.
1,384 citations
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TL;DR: It is reported that expression of wild-type but not of mutated SIP1 downregulates mammalian E-cadherin transcription via binding to both conserved E2 boxes of the minimal E- cadheringin promoter.
1,369 citations
Authors
Showing all 19431 results
Name | H-index | Papers | Citations |
---|---|---|---|
Robert J. Lefkowitz | 214 | 860 | 147995 |
Ronald M. Evans | 199 | 708 | 166722 |
Tony Hunter | 175 | 593 | 124726 |
Marc G. Caron | 173 | 674 | 99802 |
Mark Gerstein | 168 | 751 | 149578 |
Timothy A. Springer | 167 | 669 | 122421 |
Harvey F. Lodish | 165 | 782 | 101124 |
Ira Pastan | 160 | 1286 | 110069 |
Bruce N. Ames | 158 | 506 | 129010 |
Philip Cohen | 154 | 555 | 110856 |
Gerald M. Rubin | 152 | 382 | 115248 |
Ashok Kumar | 151 | 5654 | 164086 |
Kim Nasmyth | 142 | 294 | 59231 |
Kenneth M. Yamada | 139 | 446 | 72136 |
Harold E. Varmus | 137 | 496 | 76320 |