ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Articles  (268)
  • Signal Transduction
  • Nature Publishing Group (NPG)  (268)
  • Natural Sciences in General  (268)
  • Energy, Environment Protection, Nuclear Power Engineering
Collection
  • Articles  (268)
Publisher
Years
Topic
  • 11
    Publication Date: 2015-12-18
    Description: Variant rs351855-G/A is a commonly occurring single-nucleotide polymorphism of coding regions in exon 9 of the fibroblast growth factor receptor FGFR4 (CD334) gene (c.1162G〉A). It results in an amino-acid change at codon 388 from glycine to arginine (p.Gly388Arg) in the transmembrane domain of the receptor. Despite compelling genetic evidence for the association of this common variant with cancers of the bone, breast, colon, prostate, skin, lung, head and neck, as well as soft-tissue sarcomas and non-Hodgkin lymphoma, the underlying biological mechanism has remained elusive. Here we show that substitution of the conserved glycine 388 residue to a charged arginine residue alters the transmembrane spanning segment and exposes a membrane-proximal cytoplasmic signal transducer and activator of transcription 3 (STAT3) binding site Y(390)-(P)XXQ(393). We demonstrate that such membrane-proximal STAT3 binding motifs in the germline of type I membrane receptors enhance STAT3 tyrosine phosphorylation by recruiting STAT3 proteins to the inner cell membrane. Remarkably, such germline variants frequently co-localize with somatic mutations in the Catalogue of Somatic Mutations in Cancer (COSMIC) database. Using Fgfr4 single nucleotide polymorphism knock-in mice and transgenic mouse models for breast and lung cancers, we validate the enhanced STAT3 signalling induced by the FGFR4 Arg388-variant in vivo. Thus, our findings elucidate the molecular mechanism behind the genetic association of rs351855 with accelerated cancer progression and suggest that germline variants of cell-surface molecules that recruit STAT3 to the inner cell membrane are a significant risk for cancer prognosis and disease progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ulaganathan, Vijay K -- Sperl, Bianca -- Rapp, Ulf R -- Ullrich, Axel -- HL-102923/HL/NHLBI NIH HHS/ -- HL-102924/HL/NHLBI NIH HHS/ -- HL-102925/HL/NHLBI NIH HHS/ -- HL-102926/HL/NHLBI NIH HHS/ -- HL-103010/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Dec 24;528(7583):570-4. doi: 10.1038/nature16449. Epub 2015 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Biochemistry, Department of Molecular Biology, Am Klopferspitz 18, 82152, Martinsried. Germany. ; Max Planck Institute for Heart and Lung Research, Molecular Mechanisms of Lung Cancer, Parkstrasse 1, 61231 Bad Nauheim, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26675719" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs/genetics ; Amino Acid Sequence ; Animals ; Binding Sites/genetics ; Breast Neoplasms/genetics/metabolism ; Cell Line ; Cell Membrane/*metabolism ; Disease Models, Animal ; Disease Progression ; Exons/genetics ; Female ; Gene Knock-In Techniques ; *Germ-Line Mutation ; Humans ; Lung Neoplasms/genetics/metabolism ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Phosphorylation ; Phosphotyrosine/metabolism ; Polymorphism, Single Nucleotide/genetics ; Receptor, Fibroblast Growth Factor, Type 4/chemistry/*genetics/*metabolism ; STAT3 Transcription Factor/*metabolism ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 12
    Publication Date: 2015-12-10
    Description: Epithelial regeneration is critical for barrier maintenance and organ function after intestinal injury. The intestinal stem cell (ISC) niche provides Wnt, Notch and epidermal growth factor (EGF) signals supporting Lgr5(+) crypt base columnar ISCs for normal epithelial maintenance. However, little is known about the regulation of the ISC compartment after tissue damage. Using ex vivo organoid cultures, here we show that innate lymphoid cells (ILCs), potent producers of interleukin-22 (IL-22) after intestinal injury, increase the growth of mouse small intestine organoids in an IL-22-dependent fashion. Recombinant IL-22 directly targeted ISCs, augmenting the growth of both mouse and human intestinal organoids, increasing proliferation and promoting ISC expansion. IL-22 induced STAT3 phosphorylation in Lgr5(+) ISCs, and STAT3 was crucial for both organoid formation and IL-22-mediated regeneration. Treatment with IL-22 in vivo after mouse allogeneic bone marrow transplantation enhanced the recovery of ISCs, increased epithelial regeneration and reduced intestinal pathology and mortality from graft-versus-host disease. ATOH1-deficient organoid culture demonstrated that IL-22 induced epithelial regeneration independently of the Paneth cell niche. Our findings reveal a fundamental mechanism by which the immune system is able to support the intestinal epithelium, activating ISCs to promote regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720437/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720437/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lindemans, Caroline A -- Calafiore, Marco -- Mertelsmann, Anna M -- O'Connor, Margaret H -- Dudakov, Jarrod A -- Jenq, Robert R -- Velardi, Enrico -- Young, Lauren F -- Smith, Odette M -- Lawrence, Gillian -- Ivanov, Juliet A -- Fu, Ya-Yuan -- Takashima, Shuichiro -- Hua, Guoqiang -- Martin, Maria L -- O'Rourke, Kevin P -- Lo, Yuan-Hung -- Mokry, Michal -- Romera-Hernandez, Monica -- Cupedo, Tom -- Dow, Lukas E -- Nieuwenhuis, Edward E -- Shroyer, Noah F -- Liu, Chen -- Kolesnick, Richard -- van den Brink, Marcel R M -- Hanash, Alan M -- HHSN272200900059C/PHS HHS/ -- K08 HL115355/HL/NHLBI NIH HHS/ -- K08-HL115355/HL/NHLBI NIH HHS/ -- K99 CA176376/CA/NCI NIH HHS/ -- K99-CA176376/CA/NCI NIH HHS/ -- P01 CA023766/CA/NCI NIH HHS/ -- P01-CA023766/CA/NCI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- P30-CA008748/CA/NCI NIH HHS/ -- R01 AI080455/AI/NIAID NIH HHS/ -- R01 AI100288/AI/NIAID NIH HHS/ -- R01 AI101406/AI/NIAID NIH HHS/ -- R01 HL069929/HL/NHLBI NIH HHS/ -- R01 HL125571/HL/NHLBI NIH HHS/ -- R01-AI080455/AI/NIAID NIH HHS/ -- R01-AI100288/AI/NIAID NIH HHS/ -- R01-AI101406/AI/NIAID NIH HHS/ -- R01-HL069929/HL/NHLBI NIH HHS/ -- R01-HL125571/HL/NHLBI NIH HHS/ -- U19 AI116497/AI/NIAID NIH HHS/ -- England -- Nature. 2015 Dec 24;528(7583):560-4. doi: 10.1038/nature16460. Epub 2015 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Pediatrics, University Medical Center Utrecht, 3508 AB Utrecht, The Netherlands. ; Department of Immunology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Anatomy and Developmental Biology, Monash University, Clayton 3800, Australia. ; Department of Medicine, Weill Cornell Medicine, New York, New York 10021, USA. ; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Molecular Pharmacology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Cancer Biology &Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Hematology, Erasmus University Medical Center, 3000 CA Rotterdam, The Netherlands. ; Department of Pathology, Immunology and Laboratory Medicine, University of Florida College of Medicine, Gainesville, Florida 32610, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26649819" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Epithelial Cells/*cytology/immunology/pathology ; Female ; Graft vs Host Disease/pathology ; Humans ; Immunity, Mucosal ; Interleukins/deficiency/*immunology ; Intestinal Mucosa/*cytology/immunology/pathology ; Intestine, Small/*cytology/immunology/pathology ; Mice ; Organoids/cytology/growth & development/immunology ; Paneth Cells/cytology ; Phosphorylation ; *Regeneration ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Stem Cell Niche ; Stem Cells/*cytology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 13
    Publication Date: 2015-12-10
    Description: Inactivation of the TNFAIP3 gene, encoding the A20 protein, is associated with critical inflammatory diseases including multiple sclerosis, rheumatoid arthritis and Crohn's disease. However, the role of A20 in attenuating inflammatory signalling is unclear owing to paradoxical in vitro and in vivo findings. Here we utilize genetically engineered mice bearing mutations in the A20 ovarian tumour (OTU)-type deubiquitinase domain or in the zinc finger-4 (ZnF4) ubiquitin-binding motif to investigate these discrepancies. We find that phosphorylation of A20 promotes cleavage of Lys63-linked polyubiquitin chains by the OTU domain and enhances ZnF4-mediated substrate ubiquitination. Additionally, levels of linear ubiquitination dictate whether A20-deficient cells die in response to tumour necrosis factor. Mechanistically, linear ubiquitin chains preserve the architecture of the TNFR1 signalling complex by blocking A20-mediated disassembly of Lys63-linked polyubiquitin scaffolds. Collectively, our studies reveal molecular mechanisms whereby A20 deubiquitinase activity and ubiquitin binding, linear ubiquitination, and cellular kinases cooperate to regulate inflammation and cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wertz, Ingrid E -- Newton, Kim -- Seshasayee, Dhaya -- Kusam, Saritha -- Lam, Cynthia -- Zhang, Juan -- Popovych, Nataliya -- Helgason, Elizabeth -- Schoeffler, Allyn -- Jeet, Surinder -- Ramamoorthi, Nandhini -- Kategaya, Lorna -- Newman, Robert J -- Horikawa, Keisuke -- Dugger, Debra -- Sandoval, Wendy -- Mukund, Susmith -- Zindal, Anuradha -- Martin, Flavius -- Quan, Clifford -- Tom, Jeffrey -- Fairbrother, Wayne J -- Townsend, Michael -- Warming, Soren -- DeVoss, Jason -- Liu, Jinfeng -- Dueber, Erin -- Caplazi, Patrick -- Lee, Wyne P -- Goodnow, Christopher C -- Balazs, Mercedesz -- Yu, Kebing -- Kolumam, Ganesh -- Dixit, Vishva M -- England -- Nature. 2015 Dec 17;528(7582):370-5. doi: 10.1038/nature16165. Epub 2015 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Discovery Oncology, Genentech, South San Francisco, California 94080, USA. ; Early Discovery Biochemistry, Genentech, South San Francisco, California 94080, USA. ; Physiological Chemistry, Genentech, South San Francisco, California 94080, USA. ; Immunology, Genentech, South San Francisco, California 94080, USA. ; Molecular Biology, Genentech, South San Francisco, California 94080, USA. ; Department of Cancer Biology and Therapeutics, The John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory 2601, Australia. ; Protein Chemistry, Genentech, South San Francisco, California 94080, USA. ; Structural Biology, Genentech, South San Francisco, California 94080, USA. ; Bioinformatics, Genentech, South San Francisco, California 94080, USA. ; Pathology, Genentech, South San Francisco, California 94080, USA. ; Immunogenomics Laboratory, Immunology Division, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, New South Wales 2010, Sydney, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26649818" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death ; Cysteine Endopeptidases/chemistry/genetics/*metabolism ; Female ; Inflammation/genetics/*metabolism/pathology ; Intracellular Signaling Peptides and Proteins/chemistry/genetics/*metabolism ; Lysine/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Phosphorylation ; Polyubiquitin/chemistry/metabolism ; Protein Binding ; Protein Kinases/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/metabolism ; Ubiquitin/*chemistry/*metabolism ; Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 14
    Publication Date: 2015-11-26
    Description: T-cell receptor (TCR) signalling has a key role in determining T-cell fate. Precursor cells expressing TCRs within a certain low-affinity range for complexes of self-peptide and major histocompatibility complex (MHC) undergo positive selection and differentiate into naive T cells expressing a highly diverse self-MHC-restricted TCR repertoire. In contrast, precursors displaying TCRs with a high affinity for 'self' are either eliminated through TCR-agonist-induced apoptosis (negative selection) or restrained by regulatory T (Treg) cells, whose differentiation and function are controlled by the X-chromosome-encoded transcription factor Foxp3 (reviewed in ref. 2). Foxp3 is expressed in a fraction of self-reactive T cells that escape negative selection in response to agonist-driven TCR signals combined with interleukin 2 (IL-2) receptor signalling. In addition to Treg cells, TCR-agonist-driven selection results in the generation of several other specialized T-cell lineages such as natural killer T cells and innate mucosal-associated invariant T cells. Although the latter exhibit a restricted TCR repertoire, Treg cells display a highly diverse collection of TCRs. Here we explore in mice whether a specialized mechanism enables agonist-driven selection of Treg cells with a diverse TCR repertoire, and the importance this holds for self-tolerance. We show that the intronic Foxp3 enhancer conserved noncoding sequence 3 (CNS3) acts as an epigenetic switch that confers a poised state to the Foxp3 promoter in precursor cells to make Treg cell lineage commitment responsive to a broad range of TCR stimuli, particularly to suboptimal ones. CNS3-dependent expansion of the TCR repertoire enables Treg cells to control self-reactive T cells effectively, especially when thymic negative selection is genetically impaired. Our findings highlight the complementary roles of these two main mechanisms of self-tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, Yongqiang -- van der Veeken, Joris -- Shugay, Mikhail -- Putintseva, Ekaterina V -- Osmanbeyoglu, Hatice U -- Dikiy, Stanislav -- Hoyos, Beatrice E -- Moltedo, Bruno -- Hemmers, Saskia -- Treuting, Piper -- Leslie, Christina S -- Chudakov, Dmitriy M -- Rudensky, Alexander Y -- P30 CA008748/CA/NCI NIH HHS/ -- R01 AI034206/AI/NIAID NIH HHS/ -- R37 AI034206/AI/NIAID NIH HHS/ -- U01 HG007893/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Dec 3;528(7580):132-6. doi: 10.1038/nature16141. Epub 2015 Nov 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Immunology Program, Ludwig Center at Memorial Sloan Kettering Cancer Center, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry RAS, Miklukho-Maklaya 16/10, Moscow 117997, Russia. ; Pirogov Russian National Research Medical University, Ostrovityanova 1, Moscow 117997, Russia. ; Central European Institute of Technology, Masaryk University, Kamenice 753/5, Brno 62500, Czech Republic. ; Computational Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Comparative Medicine, School of Medicine, University of Washington, Seattle, Washington 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26605529" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Conserved Sequence/genetics ; Enhancer Elements, Genetic/genetics ; Epigenesis, Genetic ; Female ; Forkhead Transcription Factors/genetics ; Introns/genetics ; Male ; Mice ; Promoter Regions, Genetic/genetics ; Receptors, Antigen, T-Cell/genetics/metabolism ; Receptors, Interleukin-2/immunology/metabolism ; Self Tolerance/*immunology ; Signal Transduction ; T-Lymphocytes, Regulatory/*cytology/*immunology/metabolism ; Transcription Factors/deficiency
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 15
    Publication Date: 2015-11-19
    Description: Acorn worms, also known as enteropneust (literally, 'gut-breathing') hemichordates, are marine invertebrates that share features with echinoderms and chordates. Together, these three phyla comprise the deuterostomes. Here we report the draft genome sequences of two acorn worms, Saccoglossus kowalevskii and Ptychodera flava. By comparing them with diverse bilaterian genomes, we identify shared traits that were probably inherited from the last common deuterostome ancestor, and then explore evolutionary trajectories leading from this ancestor to hemichordates, echinoderms and chordates. The hemichordate genomes exhibit extensive conserved synteny with amphioxus and other bilaterians, and deeply conserved non-coding sequences that are candidates for conserved gene-regulatory elements. Notably, hemichordates possess a deuterostome-specific genomic cluster of four ordered transcription factor genes, the expression of which is associated with the development of pharyngeal 'gill' slits, the foremost morphological innovation of early deuterostomes, and is probably central to their filter-feeding lifestyle. Comparative analysis reveals numerous deuterostome-specific gene novelties, including genes found in deuterostomes and marine microbes, but not other animals. The putative functions of these genes can be linked to physiological, metabolic and developmental specializations of the filter-feeding ancestor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4729200/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4729200/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simakov, Oleg -- Kawashima, Takeshi -- Marletaz, Ferdinand -- Jenkins, Jerry -- Koyanagi, Ryo -- Mitros, Therese -- Hisata, Kanako -- Bredeson, Jessen -- Shoguchi, Eiichi -- Gyoja, Fuki -- Yue, Jia-Xing -- Chen, Yi-Chih -- Freeman, Robert M Jr -- Sasaki, Akane -- Hikosaka-Katayama, Tomoe -- Sato, Atsuko -- Fujie, Manabu -- Baughman, Kenneth W -- Levine, Judith -- Gonzalez, Paul -- Cameron, Christopher -- Fritzenwanker, Jens H -- Pani, Ariel M -- Goto, Hiroki -- Kanda, Miyuki -- Arakaki, Nana -- Yamasaki, Shinichi -- Qu, Jiaxin -- Cree, Andrew -- Ding, Yan -- Dinh, Huyen H -- Dugan, Shannon -- Holder, Michael -- Jhangiani, Shalini N -- Kovar, Christie L -- Lee, Sandra L -- Lewis, Lora R -- Morton, Donna -- Nazareth, Lynne V -- Okwuonu, Geoffrey -- Santibanez, Jireh -- Chen, Rui -- Richards, Stephen -- Muzny, Donna M -- Gillis, Andrew -- Peshkin, Leonid -- Wu, Michael -- Humphreys, Tom -- Su, Yi-Hsien -- Putnam, Nicholas H -- Schmutz, Jeremy -- Fujiyama, Asao -- Yu, Jr-Kai -- Tagawa, Kunifumi -- Worley, Kim C -- Gibbs, Richard A -- Kirschner, Marc W -- Lowe, Christopher J -- Satoh, Noriyuki -- Rokhsar, Daniel S -- Gerhart, John -- HD37277/HD/NICHD NIH HHS/ -- HD42724/HD/NICHD NIH HHS/ -- R01 HD037277/HD/NICHD NIH HHS/ -- R01 HD073104/HD/NICHD NIH HHS/ -- R01HD073104/HD/NICHD NIH HHS/ -- T32 HD055164/HD/NICHD NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- England -- Nature. 2015 Nov 26;527(7579):459-65. doi: 10.1038/nature16150. Epub 2015 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Unit, Okinawa Institute of Science and Technology Graduate University, Onna, Okinawa 904-0495, Japan. ; Department of Molecular Evolution, Centre for Organismal Studies, University of Heidelberg, 69115 Heidelberg, Germany. ; Marine Genomics Unit, Okinawa Institute of Science and Technology Graduate University, Onna, Okinawa 904-0495, Japan. ; Department of Zoology, University of Oxford, Oxford OX1 3PS, UK. ; HudsonAlpha Institute of Biotechnology, Huntsville, Alabama 35806, USA. ; DNA Sequencing Section, Okinawa Institute of Science and Technology Graduate University, Onna, Okinawa 904-0495, Japan. ; Department of Molecular and Cell Biology, University of California, Berkeley California 94720-3200, USA. ; Department of Ecology and Evolutionary Biology, Rice University, Houston, Texas 77005, USA. ; Institute of Cellular and Organismic Biology, Academia Sinica, Taipei 11529, Taiwan. ; Department of Systems Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Marine Biological Laboratory, Graduate School of Science, Hiroshima University, Onomichi, Hiroshima 722-0073, Japan. ; Natural Science Center for Basic Research and Development, Gene Science Division, Hiroshima University, Higashi-Hiroshima, Hiroshima 739-8527, Japan. ; Marine Biological Association of the UK, The Laboratory, Citadel Hill, Plymouth PL1 2PB, UK. ; Department of Biology, Hopkins Marine Station, Stanford University, Pacific Grove, California 93950, USA. ; Department de sciences biologiques, University of Montreal, Quebec H3C 3J7, Canada. ; University of North Caroline at Chapel Hill, North Carolina 27599, USA. ; Human Genome Sequencing Center, Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, MS BCM226, Houston, Texas 77030, USA. ; Department of Zoology, University of Cambridge, Cambridge CB2 3EJ, UK. ; Institute for Biogenesis Research, University of Hawaii, Hawaii 96822, USA. ; National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan. ; US Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26580012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chordata, Nonvertebrate/classification/*genetics ; Conserved Sequence/genetics ; Echinodermata/classification/genetics ; *Evolution, Molecular ; Genome/*genetics ; Multigene Family/genetics ; Phylogeny ; Signal Transduction ; Synteny/genetics ; Transforming Growth Factor beta
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 16
    Publication Date: 2015-11-10
    Description: Drosophila Decapentaplegic (Dpp) has served as a paradigm to study morphogen-dependent growth control. However, the role of a Dpp gradient in tissue growth remains highly controversial. Two fundamentally different models have been proposed: the 'temporal rule' model suggests that all cells of the wing imaginal disc divide upon a 50% increase in Dpp signalling, whereas the 'growth equalization model' suggests that Dpp is only essential for proliferation control of the central cells. Here, to discriminate between these two models, we generated and used morphotrap, a membrane-tethered anti-green fluorescent protein (GFP) nanobody, which enables immobilization of enhanced (e)GFP::Dpp on the cell surface, thereby abolishing Dpp gradient formation. We find that in the absence of Dpp spreading, wing disc patterning is lost; however, lateral cells still divide at normal rates. These data are consistent with the growth equalization model, but do not fit a global temporal rule model in the wing imaginal disc.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harmansa, Stefan -- Hamaratoglu, Fisun -- Affolter, Markus -- Caussinus, Emmanuel -- England -- Nature. 2015 Nov 19;527(7578):317-22. doi: 10.1038/nature15712. Epub 2015 Nov 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Growth &Development, Biozentrum, Klingelbergstrasse 50/70, University of Basel, 4056 Basel, Switzerland. ; Center for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland. ; Institute of Molecular Life Sciences (IMLS), University of Zurich, 8057 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26550827" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning/*physiology ; Cell Proliferation ; DNA-Binding Proteins/metabolism ; Drosophila Proteins/*metabolism ; Drosophila melanogaster/cytology/*growth & development/*metabolism ; Male ; Repressor Proteins/metabolism ; Signal Transduction ; Single-Chain Antibodies ; Transcription Factors/metabolism ; Wings, Animal/cytology/*growth & development/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 17
    Publication Date: 2015-10-28
    Description: The study of bacterial ion channels has provided fundamental insights into the structural basis of neuronal signalling; however, the native role of ion channels in bacteria has remained elusive. Here we show that ion channels conduct long-range electrical signals within bacterial biofilm communities through spatially propagating waves of potassium. These waves result from a positive feedback loop, in which a metabolic trigger induces release of intracellular potassium, which in turn depolarizes neighbouring cells. Propagating through the biofilm, this wave of depolarization coordinates metabolic states among cells in the interior and periphery of the biofilm. Deletion of the potassium channel abolishes this response. As predicted by a mathematical model, we further show that spatial propagation can be hindered by specific genetic perturbations to potassium channel gating. Together, these results demonstrate a function for ion channels in bacterial biofilms, and provide a prokaryotic paradigm for active, long-range electrical signalling in cellular communities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prindle, Arthur -- Liu, Jintao -- Asally, Munehiro -- Ly, San -- Garcia-Ojalvo, Jordi -- Suel, Gurol M -- P50 GM085764/GM/NIGMS NIH HHS/ -- R01GM088428/GM/NIGMS NIH HHS/ -- England -- Nature. 2015 Nov 5;527(7576):59-63. doi: 10.1038/nature15709. Epub 2015 Oct 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Sciences, University of California San Diego, California 92093, USA. ; Warwick Integrative Synthetic Biology Centre, School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK. ; Department of Experimental and Health Sciences, Universitat Pompeu Fabra, 08003 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26503040" target="_blank"〉PubMed〈/a〉
    Keywords: Bacillus subtilis/*cytology/growth & development/*metabolism ; Biofilms/*growth & development ; *Electric Conductivity ; Feedback, Physiological ; Ion Channel Gating ; Membrane Potentials ; Models, Biological ; Potassium/metabolism ; Potassium Channels/*metabolism ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 18
    Publication Date: 2015-10-16
    Description: Studies of individual living cells have revealed that many transcription factors activate in dynamic, and often stochastic, pulses within the same cell. However, it has remained unclear whether cells might exploit the dynamic interaction of these pulses to control gene expression. Here, using quantitative single-cell time-lapse imaging of Saccharomyces cerevisiae, we show that the pulsatile transcription factors Msn2 and Mig1 combinatorially regulate their target genes through modulation of their relative pulse timing. The activator Msn2 and repressor Mig1 showed pulsed activation in either a temporally overlapping or non-overlapping manner during their transient response to different inputs, with only the non-overlapping dynamics efficiently activating target gene expression. Similarly, under constant environmental conditions, where Msn2 and Mig1 exhibit sporadic pulsing, glucose concentration modulated the temporal overlap between pulses of the two factors. Together, these results reveal a time-based mode of combinatorial gene regulation. Regulation through relative signal timing is common in engineering and neurobiology, and these results suggest that it could also function broadly within the signalling and regulatory systems of the cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Yihan -- Sohn, Chang Ho -- Dalal, Chiraj K -- Cai, Long -- Elowitz, Michael B -- R01 GM079771/GM/NIGMS NIH HHS/ -- R01 GM079771B/GM/NIGMS NIH HHS/ -- R01 GM086793/GM/NIGMS NIH HHS/ -- R01 GM086793A/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Nov 5;527(7576):54-8. doi: 10.1038/nature15710. Epub 2015 Oct 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125, USA. ; Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, California 91125, USA. ; Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, California 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26466562" target="_blank"〉PubMed〈/a〉
    Keywords: DNA-Binding Proteins/metabolism ; *Gene Expression Regulation, Fungal ; Glucose/deficiency/metabolism ; Repressor Proteins/metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; Signal Transduction ; Single-Cell Analysis ; Time Factors ; Time-Lapse Imaging ; Transcription Factors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 19
    Publication Date: 2015-09-17
    Description: Blood polymorphonuclear neutrophils provide immune protection against pathogens, but may also promote tissue injury in inflammatory diseases. Although neutrophils are generally considered to be a relatively homogeneous population, evidence for heterogeneity is emerging. Under steady-state conditions, neutrophil heterogeneity may arise from ageing and replenishment by newly released neutrophils from the bone marrow. Aged neutrophils upregulate CXCR4, a receptor allowing their clearance in the bone marrow, with feedback inhibition of neutrophil production via the IL-17/G-CSF axis, and rhythmic modulation of the haematopoietic stem-cell niche. The aged subset also expresses low levels of L-selectin. Previous studies have suggested that in vitro-aged neutrophils exhibit impaired migration and reduced pro-inflammatory properties. Here, using in vivo ageing analyses in mice, we show that neutrophil pro-inflammatory activity correlates positively with their ageing whilst in circulation. Aged neutrophils represent an overly active subset exhibiting enhanced alphaMbeta2 integrin activation and neutrophil extracellular trap formation under inflammatory conditions. Neutrophil ageing is driven by the microbiota via Toll-like receptor and myeloid differentiation factor 88-mediated signalling pathways. Depletion of the microbiota significantly reduces the number of circulating aged neutrophils and dramatically improves the pathogenesis and inflammation-related organ damage in models of sickle-cell disease or endotoxin-induced septic shock. These results identify a role for the microbiota in regulating a disease-promoting neutrophil subset.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4712631/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4712631/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Dachuan -- Chen, Grace -- Manwani, Deepa -- Mortha, Arthur -- Xu, Chunliang -- Faith, Jeremiah J -- Burk, Robert D -- Kunisaki, Yuya -- Jang, Jung-Eun -- Scheiermann, Christoph -- Merad, Miriam -- Frenette, Paul S -- R01 CA154947/CA/NCI NIH HHS/ -- R01 CA173861/CA/NCI NIH HHS/ -- R01 CA190400/CA/NCI NIH HHS/ -- R01 DK056638/DK/NIDDK NIH HHS/ -- R01 HL069438/HL/NHLBI NIH HHS/ -- R01 HL116340/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Sep 24;525(7570):528-32. doi: 10.1038/nature15367. Epub 2015 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Pediatrics, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York 10029, USA. ; The Immunology Institute, Mount Sinai School of Medicine, New York, New York 10029, USA. ; The Institute for Genomics and Multiscale Biology, Mount Sinai School of Medicine, New York, New York 10029, USA. ; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26374999" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/blood/microbiology/pathology ; Animals ; Cell Aging/*immunology ; Disease Models, Animal ; Erythrocytes, Abnormal/pathology ; Inflammation/immunology/pathology ; Macrophage-1 Antigen/metabolism ; Male ; Mice ; Microbiota/*immunology ; Myeloid Differentiation Factor 88/metabolism ; Neutrophils/*cytology/*immunology ; Shock, Septic/immunology/microbiology/pathology ; Signal Transduction ; Toll-Like Receptors/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 20
    Publication Date: 2015-09-17
    Description: The elucidation of factors that activate the regeneration of the adult mammalian heart is of major scientific and therapeutic importance. Here we found that epicardial cells contain a potent cardiogenic activity identified as follistatin-like 1 (Fstl1). Epicardial Fstl1 declines following myocardial infarction and is replaced by myocardial expression. Myocardial Fstl1 does not promote regeneration, either basally or upon transgenic overexpression. Application of the human Fstl1 protein (FSTL1) via an epicardial patch stimulates cell cycle entry and division of pre-existing cardiomyocytes, improving cardiac function and survival in mouse and swine models of myocardial infarction. The data suggest that the loss of epicardial FSTL1 is a maladaptive response to injury, and that its restoration would be an effective way to reverse myocardial death and remodelling following myocardial infarction in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4762253/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4762253/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wei, Ke -- Serpooshan, Vahid -- Hurtado, Cecilia -- Diez-Cunado, Marta -- Zhao, Mingming -- Maruyama, Sonomi -- Zhu, Wenhong -- Fajardo, Giovanni -- Noseda, Michela -- Nakamura, Kazuto -- Tian, Xueying -- Liu, Qiaozhen -- Wang, Andrew -- Matsuura, Yuka -- Bushway, Paul -- Cai, Wenqing -- Savchenko, Alex -- Mahmoudi, Morteza -- Schneider, Michael D -- van den Hoff, Maurice J B -- Butte, Manish J -- Yang, Phillip C -- Walsh, Kenneth -- Zhou, Bin -- Bernstein, Daniel -- Mercola, Mark -- Ruiz-Lozano, Pilar -- 5UM1 HL113456/HL/NHLBI NIH HHS/ -- HL065484/HL/NHLBI NIH HHS/ -- HL108176/HL/NHLBI NIH HHS/ -- HL113601/HL/NHLBI NIH HHS/ -- HL116591/HL/NHLBI NIH HHS/ -- K08 AI079268/AI/NIAID NIH HHS/ -- P01 HL098053/HL/NHLBI NIH HHS/ -- P30 AR061303/AR/NIAMS NIH HHS/ -- P30 CA030199/CA/NCI NIH HHS/ -- R01 HL086879/HL/NHLBI NIH HHS/ -- R01 HL113601/HL/NHLBI NIH HHS/ -- UM1 HL113456/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Sep 24;525(7570):479-85. doi: 10.1038/nature15372. Epub 2015 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, University of California, San Diego, La Jolla, California 92037, USA. ; Sanford-Burnham-Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, California 92037, USA. ; Stanford Cardiovascular Institute and Department of Pediatrics, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305, USA. ; Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA. ; Imperial College London, Faculty of Medicine, Imperial Centre for Translational and Experimental Medicine, Du Cane Road, London W12 0NN, UK. ; Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, and Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. ; Nanotechnology Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, 1417613151 Tehran, Iran. ; Academic Medical Center. Dept Anatomy, Embryology and Physiology. Meibergdreef 15. 1105AZ Amsterdam, The Netherlands. ; CAS Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26375005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Proliferation/drug effects ; Culture Media, Conditioned/pharmacology ; Female ; Follistatin-Related Proteins/genetics/*metabolism ; Humans ; Male ; Mice ; Myoblasts, Cardiac/cytology/drug effects ; Myocardial Infarction/genetics/metabolism/pathology/physiopathology ; Myocardium/*metabolism ; Myocytes, Cardiac/cytology/drug effects/metabolism ; Pericardium/cytology/drug effects/*growth & development/*metabolism ; Rats ; *Regeneration/drug effects ; Signal Transduction ; Swine ; Transgenes/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...