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  • Oxford University Press  (33)
  • Nature Publishing Group (NPG)  (5)
  • American Meteorological Society (AMS)
  • Cambridge University Press
  • 2005-2009  (40)
  • 1990-1994
  • 2009  (40)
Collection
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  • 2005-2009  (40)
  • 1990-1994
Year
  • 1
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    Force-induced activation of covalent bonds in mechanoresponsive polymeric materials (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-05-09
    Description: Mechanochemical transduction enables an extraordinary range of physiological processes such as the sense of touch, hearing, balance, muscle contraction, and the growth and remodelling of tissue and bone. Although biology is replete with materials systems that actively and functionally respond to mechanical stimuli, the default mechanochemical reaction of bulk polymers to large external stress is the unselective scission of covalent bonds, resulting in damage or failure. An alternative to this degradation process is the rational molecular design of synthetic materials such that mechanical stress favourably alters material properties. A few mechanosensitive polymers with this property have been developed; but their active response is mediated through non-covalent processes, which may limit the extent to which properties can be modified and the long-term stability in structural materials. Previously, we have shown with dissolved polymer strands incorporating mechanically sensitive chemical groups-so-called mechanophores-that the directional nature of mechanical forces can selectively break and re-form covalent bonds. We now demonstrate that such force-induced covalent-bond activation can also be realized with mechanophore-linked elastomeric and glassy polymers, by using a mechanophore that changes colour as it undergoes a reversible electrocyclic ring-opening reaction under tensile stress and thus allows us to directly and locally visualize the mechanochemical reaction. We find that pronounced changes in colour and fluorescence emerge with the accumulation of plastic deformation, indicating that in these polymeric materials the transduction of mechanical force into the ring-opening reaction is an activated process. We anticipate that force activation of covalent bonds can serve as a general strategy for the development of new mechanophore building blocks that impart polymeric materials with desirable functionalities ranging from damage sensing to fully regenerative self-healing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, Douglas A -- Hamilton, Andrew -- Yang, Jinglei -- Cremar, Lee D -- Van Gough, Dara -- Potisek, Stephanie L -- Ong, Mitchell T -- Braun, Paul V -- Martinez, Todd J -- White, Scott R -- Moore, Jeffrey S -- Sottos, Nancy R -- England -- Nature. 2009 May 7;459(7243):68-72. doi: 10.1038/nature07970.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Illinois at Urbana-Champaign, Illinois 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19424152" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Weapons: the need to replace ageing and deteriorating stock (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-11-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, Jay -- England -- Nature. 2009 Nov 12;462(7270):158. doi: 10.1038/462158a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19907473" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Direct inhibition of the NOTCH transcription factor complex (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-11-13
    Description: Direct inhibition of transcription factor complexes remains a central challenge in the discipline of ligand discovery. In general, these proteins lack surface involutions suitable for high-affinity binding by small molecules. Here we report the design of synthetic, cell-permeable, stabilized alpha-helical peptides that target a critical protein-protein interface in the NOTCH transactivation complex. We demonstrate that direct, high-affinity binding of the hydrocarbon-stapled peptide SAHM1 prevents assembly of the active transcriptional complex. Inappropriate NOTCH activation is directly implicated in the pathogenesis of several disease states, including T-cell acute lymphoblastic leukaemia (T-ALL). The treatment of leukaemic cells with SAHM1 results in genome-wide suppression of NOTCH-activated genes. Direct antagonism of the NOTCH transcriptional program causes potent, NOTCH-specific anti-proliferative effects in cultured cells and in a mouse model of NOTCH1-driven T-ALL.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2951323/" 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/PMC2951323/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moellering, Raymond E -- Cornejo, Melanie -- Davis, Tina N -- Del Bianco, Cristina -- Aster, Jon C -- Blacklow, Stephen C -- Kung, Andrew L -- Gilliland, D Gary -- Verdine, Gregory L -- Bradner, James E -- 5T32GM007598/GM/NIGMS NIH HHS/ -- N01-CO-12400/CO/NCI NIH HHS/ -- P01 CA119070/CA/NCI NIH HHS/ -- P01 CA119070-049001/CA/NCI NIH HHS/ -- R01 CA092433/CA/NCI NIH HHS/ -- R01 CA092433-06A2/CA/NCI NIH HHS/ -- R56 CA092433/CA/NCI NIH HHS/ -- R56 CA092433-06A1/CA/NCI NIH HHS/ -- T32 GM007598/GM/NIGMS NIH HHS/ -- T32 GM007598-30/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Nov 12;462(7270):182-8. doi: 10.1038/nature08543.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry & Chemical Biology, Harvard University, Cambridge, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19907488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding, Competitive ; Cell Line, Tumor ; Cell Membrane Permeability ; Cell Proliferation/drug effects ; DNA-Binding Proteins/chemistry/metabolism ; Disease Models, Animal ; Drosophila Proteins/chemistry ; Gene Expression Regulation, Neoplastic/drug effects ; Genome/drug effects/genetics ; Humans ; Immunoglobulin J Recombination Signal Sequence-Binding Protein/metabolism ; Mice ; Models, Molecular ; Nuclear Proteins/chemistry ; Peptides/chemical synthesis/chemistry/metabolism/*pharmacology ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy/genetics/pathology ; Protein Binding/drug effects ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Receptor, Notch1/*antagonists & inhibitors/chemistry/metabolism ; Signal Transduction/drug effects ; Substrate Specificity ; Transcription Factors/chemistry/metabolism ; Transcriptional Activation/*drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Casein kinase 1alpha governs antigen-receptor-induced NF-kappaB activation and human lymphoma cell survival (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-01-02
    Description: The transcription factor NF-kappaB is required for lymphocyte activation and proliferation as well as the survival of certain lymphoma types. Antigen receptor stimulation assembles an NF-kappaB activating platform containing the scaffold protein CARMA1 (also called CARD11), the adaptor BCL10 and the paracaspase MALT1 (the CBM complex), linked to the inhibitor of NF-kappaB kinase complex, but signal transduction is not fully understood. We conducted parallel screens involving a mass spectrometry analysis of CARMA1 binding partners and an RNA interference screen for growth inhibition of the CBM-dependent 'activated B-cell-like' (ABC) subtype of diffuse large B-cell lymphoma (DLBCL). Here we report that both screens identified casein kinase 1alpha (CK1alpha) as a bifunctional regulator of NF-kappaB. CK1alpha dynamically associates with the CBM complex on T-cell-receptor (TCR) engagement to participate in cytokine production and lymphocyte proliferation. However, CK1alpha kinase activity has a contrasting role by subsequently promoting the phosphorylation and inactivation of CARMA1. CK1alpha has thus a dual 'gating' function which first promotes and then terminates receptor-induced NF-kappaB. ABC DLBCL cells required CK1alpha for constitutive NF-kappaB activity, indicating that CK1alpha functions as a conditionally essential malignancy gene-a member of a new class of potential cancer therapeutic targets.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688735/" 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/PMC2688735/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bidere, Nicolas -- Ngo, Vu N -- Lee, Jeansun -- Collins, Cailin -- Zheng, Lixin -- Wan, Fengyi -- Davis, R Eric -- Lenz, Georg -- Anderson, D Eric -- Arnoult, Damien -- Vazquez, Aime -- Sakai, Keiko -- Zhang, Jun -- Meng, Zhaojing -- Veenstra, Timothy D -- Staudt, Louis M -- Lenardo, Michael J -- NIH0011349228/PHS HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2009 Mar 5;458(7234):92-6. doi: 10.1038/nature07613. Epub 2008 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Development Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19118383" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; CARD Signaling Adaptor Proteins/metabolism ; Casein Kinases/*metabolism ; Caspases/metabolism ; Cell Proliferation ; Cell Survival ; Cells, Cultured ; Feedback, Physiological ; Guanylate Cyclase/metabolism ; Humans ; I-kappa B Kinase/metabolism ; Jurkat Cells ; Lymphoma, Large B-Cell, Diffuse/enzymology/*metabolism/*pathology ; NF-kappa B/*metabolism ; Neoplasm Proteins/metabolism ; Protein Binding ; Receptors, Antigen/*metabolism ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Autism genome-wide copy number variation reveals ubiquitin and neuronal genes (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-05-01
    Description: Autism spectrum disorders (ASDs) are childhood neurodevelopmental disorders with complex genetic origins. Previous studies focusing on candidate genes or genomic regions have identified several copy number variations (CNVs) that are associated with an increased risk of ASDs. Here we present the results from a whole-genome CNV study on a cohort of 859 ASD cases and 1,409 healthy children of European ancestry who were genotyped with approximately 550,000 single nucleotide polymorphism markers, in an attempt to comprehensively identify CNVs conferring susceptibility to ASDs. Positive findings were evaluated in an independent cohort of 1,336 ASD cases and 1,110 controls of European ancestry. Besides previously reported ASD candidate genes, such as NRXN1 (ref. 10) and CNTN4 (refs 11, 12), several new susceptibility genes encoding neuronal cell-adhesion molecules, including NLGN1 and ASTN2, were enriched with CNVs in ASD cases compared to controls (P = 9.5 x 10(-3)). Furthermore, CNVs within or surrounding genes involved in the ubiquitin pathways, including UBE3A, PARK2, RFWD2 and FBXO40, were affected by CNVs not observed in controls (P = 3.3 x 10(-3)). We also identified duplications 55 kilobases upstream of complementary DNA AK123120 (P = 3.6 x 10(-6)). Although these variants may be individually rare, they target genes involved in neuronal cell-adhesion or ubiquitin degradation, indicating that these two important gene networks expressed within the central nervous system may contribute to the genetic susceptibility of ASD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925224/" 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/PMC2925224/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glessner, Joseph T -- Wang, Kai -- Cai, Guiqing -- Korvatska, Olena -- Kim, Cecilia E -- Wood, Shawn -- Zhang, Haitao -- Estes, Annette -- Brune, Camille W -- Bradfield, Jonathan P -- Imielinski, Marcin -- Frackelton, Edward C -- Reichert, Jennifer -- Crawford, Emily L -- Munson, Jeffrey -- Sleiman, Patrick M A -- Chiavacci, Rosetta -- Annaiah, Kiran -- Thomas, Kelly -- Hou, Cuiping -- Glaberson, Wendy -- Flory, James -- Otieno, Frederick -- Garris, Maria -- Soorya, Latha -- Klei, Lambertus -- Piven, Joseph -- Meyer, Kacie J -- Anagnostou, Evdokia -- Sakurai, Takeshi -- Game, Rachel M -- Rudd, Danielle S -- Zurawiecki, Danielle -- McDougle, Christopher J -- Davis, Lea K -- Miller, Judith -- Posey, David J -- Michaels, Shana -- Kolevzon, Alexander -- Silverman, Jeremy M -- Bernier, Raphael -- Levy, Susan E -- Schultz, Robert T -- Dawson, Geraldine -- Owley, Thomas -- McMahon, William M -- Wassink, Thomas H -- Sweeney, John A -- Nurnberger, John I -- Coon, Hilary -- Sutcliffe, James S -- Minshew, Nancy J -- Grant, Struan F A -- Bucan, Maja -- Cook, Edwin H -- Buxbaum, Joseph D -- Devlin, Bernie -- Schellenberg, Gerard D -- Hakonarson, Hakon -- 1U24MH081810/MH/NIMH NIH HHS/ -- HD055751/HD/NICHD NIH HHS/ -- HD055782-01/HD/NICHD NIH HHS/ -- HD35476/HD/NICHD NIH HHS/ -- M01 RR000064-340579/RR/NCRR NIH HHS/ -- M01 RR000064-350579/RR/NCRR NIH HHS/ -- M01 RR000064-35S10579/RR/NCRR NIH HHS/ -- M01 RR000064-35S10591/RR/NCRR NIH HHS/ -- M01 RR000064-35S10602/RR/NCRR NIH HHS/ -- M01 RR000064-35S20579/RR/NCRR NIH HHS/ -- M01 RR000064-35S20591/RR/NCRR NIH HHS/ -- M01 RR000064-35S20602/RR/NCRR NIH HHS/ -- M01 RR000064-360579/RR/NCRR NIH HHS/ -- M01 RR000064-360582/RR/NCRR NIH HHS/ -- M01 RR000064-360591/RR/NCRR NIH HHS/ -- M01 RR000064-36S10579/RR/NCRR NIH HHS/ -- M01 RR000064-36S10582/RR/NCRR NIH HHS/ -- M01 RR000064-36S10591/RR/NCRR NIH HHS/ -- M01 RR000064-370579/RR/NCRR NIH HHS/ -- M01 RR000064-370582/RR/NCRR NIH HHS/ -- M01 RR000064-370591/RR/NCRR NIH HHS/ -- M01 RR000064-37S10579/RR/NCRR NIH HHS/ -- M01 RR000064-37S10582/RR/NCRR NIH HHS/ -- M01 RR000064-37S10591/RR/NCRR NIH HHS/ -- M01 RR000064-380579/RR/NCRR NIH HHS/ -- M01 RR000064-380582/RR/NCRR NIH HHS/ -- M01 RR000064-380591/RR/NCRR NIH HHS/ -- M01 RR000064-390579/RR/NCRR NIH HHS/ -- M01 RR000064-390582/RR/NCRR NIH HHS/ -- M01 RR000064-390591/RR/NCRR NIH HHS/ -- M01-RR00064/RR/NCRR NIH HHS/ -- MH061009/MH/NIMH NIH HHS/ -- MH0666730/MH/NIMH NIH HHS/ -- MH64547/MH/NIMH NIH HHS/ -- MH69359/MH/NIMH NIH HHS/ -- NS049261/NS/NINDS NIH HHS/ -- P01 HD035476-03/HD/NICHD NIH HHS/ -- P01 HD035476-04/HD/NICHD NIH HHS/ -- P01 HD035476-04S1/HD/NICHD NIH HHS/ -- P01 HD035476-04S2/HD/NICHD NIH HHS/ -- P01 HD035476-05/HD/NICHD NIH HHS/ -- P50 HD055751/HD/NICHD NIH HHS/ -- P50 HD055751-01/HD/NICHD NIH HHS/ -- P50 HD055751-010002/HD/NICHD NIH HHS/ -- P50 HD055751-019003/HD/NICHD NIH HHS/ -- P50 HD055751-02/HD/NICHD NIH HHS/ -- P50 HD055751-020002/HD/NICHD NIH HHS/ -- P50 HD055751-03/HD/NICHD NIH HHS/ -- P50 HD055751-030002/HD/NICHD NIH HHS/ -- P50 HD055751-04/HD/NICHD NIH HHS/ -- P50 HD055782-01/HD/NICHD NIH HHS/ -- R01 MH057881/MH/NIMH NIH HHS/ -- R01 MH061009/MH/NIMH NIH HHS/ -- R01 MH061009-01A1/MH/NIMH NIH HHS/ -- R01 MH061009-01A1S1/MH/NIMH NIH HHS/ -- R01 MH061009-02/MH/NIMH NIH HHS/ -- R01 MH061009-03/MH/NIMH NIH HHS/ -- R01 MH061009-04A1/MH/NIMH NIH HHS/ -- R01 MH061009-05/MH/NIMH NIH HHS/ -- R01 MH061009-06/MH/NIMH NIH HHS/ -- R01 MH061009-07/MH/NIMH NIH HHS/ -- R01 MH061009-08/MH/NIMH NIH HHS/ -- R01 MH064547/MH/NIMH NIH HHS/ -- R01 MH064547-01/MH/NIMH NIH HHS/ -- R01 MH064547-01S1/MH/NIMH NIH HHS/ -- R01 MH064547-02/MH/NIMH NIH HHS/ -- R01 MH064547-02S1/MH/NIMH NIH HHS/ -- R01 MH064547-03/MH/NIMH NIH HHS/ -- R01 MH064547-04/MH/NIMH NIH HHS/ -- R01 MH064547-05/MH/NIMH NIH HHS/ -- R01 MH069359/MH/NIMH NIH HHS/ -- R01 MH069359-01A2/MH/NIMH NIH HHS/ -- R01 MH069359-02/MH/NIMH NIH HHS/ -- R01 MH069359-03/MH/NIMH NIH HHS/ -- R01 MH069359-04/MH/NIMH NIH HHS/ -- R01 MH069359-05/MH/NIMH NIH HHS/ -- R01 NS049261/NS/NINDS NIH HHS/ -- R01 NS049261-01A2/NS/NINDS NIH HHS/ -- R01 NS049261-02/NS/NINDS NIH HHS/ -- R01 NS049261-03/NS/NINDS NIH HHS/ -- R01 NS049261-04/NS/NINDS NIH HHS/ -- R01 NS049261-05/NS/NINDS NIH HHS/ -- U10 MH066766-02S1/MH/NIMH NIH HHS/ -- U10MH66766-02S1/MH/NIMH NIH HHS/ -- U19 HD035476-06/HD/NICHD NIH HHS/ -- U19 HD035476-07/HD/NICHD NIH HHS/ -- U19 HD035476-08/HD/NICHD NIH HHS/ -- U19 HD035476-09/HD/NICHD NIH HHS/ -- U19 HD035476-10/HD/NICHD NIH HHS/ -- U24 MH081810/MH/NIMH NIH HHS/ -- U24 MH081810-01/MH/NIMH NIH HHS/ -- U24 MH081810-02/MH/NIMH NIH HHS/ -- U24 MH081810-03/MH/NIMH NIH HHS/ -- U24 MH081810-04/MH/NIMH NIH HHS/ -- U54 MH066673/MH/NIMH NIH HHS/ -- U54 MH066673-01A10001/MH/NIMH NIH HHS/ -- U54 MH066673-020001/MH/NIMH NIH HHS/ -- U54 MH066673-030001/MH/NIMH NIH HHS/ -- U54 MH066673-040001/MH/NIMH NIH HHS/ -- U54 MH066673-05/MH/NIMH NIH HHS/ -- U54 MH066673-050001/MH/NIMH NIH HHS/ -- UL1 RR024134/RR/NCRR NIH HHS/ -- UL1 RR024134-03/RR/NCRR NIH HHS/ -- UL1-RR024134-03/RR/NCRR NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2009 May 28;459(7246):569-73. doi: 10.1038/nature07953. Epub 2009 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Applied Genomics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19404257" target="_blank"〉PubMed〈/a〉
    Keywords: Autistic Disorder/*genetics ; Case-Control Studies ; Cell Adhesion Molecules, Neuronal/genetics ; Cohort Studies ; Europe/ethnology ; Gene Dosage/*genetics ; Gene Regulatory Networks/genetics ; Genetic Predisposition to Disease/genetics ; Genetic Variation/*genetics ; Genome, Human/*genetics ; Genotype ; Humans ; Neurons/*metabolism ; Polymerase Chain Reaction ; Polymorphism, Single Nucleotide/genetics ; Reproducibility of Results ; Ubiquitin/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Data structures and algorithms for analysis of genetics of gene expression with Bioconductor: GGtools 3.x (2009)
    Oxford University Press
    Details
    Publication Date: 2009-04-05
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
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  • 7
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    A tool for identification of genes expressed in patterns of interest using the Allen Brain Atlas (2009)
    Oxford University Press
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    Publication Date: 2009-05-04
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
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  • 8
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    Common fragile sites are characterized by histone hypoacetylation (2009)
    Oxford University Press
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    Publication Date: 2009-08-28
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
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  • 9
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    Expression differences by continent of origin point to the immortalization process (2009)
    Oxford University Press
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    Publication Date: 2009-07-23
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
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  • 10
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    MODBASE, a database of annotated comparative protein structure models and associated resources (2009)
    Oxford University Press
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    Publication Date: 2009-01-01
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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