ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    CCR3 is a target for age-related macular degeneration diagnosis and therapy (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-06-16
    Description: Age-related macular degeneration (AMD), a leading cause of blindness worldwide, is as prevalent as cancer in industrialized nations. Most blindness in AMD results from invasion of the retina by choroidal neovascularisation (CNV). Here we show that the eosinophil/mast cell chemokine receptor CCR3 is specifically expressed in choroidal neovascular endothelial cells in humans with AMD, and that despite the expression of its ligands eotaxin-1, -2 and -3, neither eosinophils nor mast cells are present in human CNV. Genetic or pharmacological targeting of CCR3 or eotaxins inhibited injury-induced CNV in mice. CNV suppression by CCR3 blockade was due to direct inhibition of endothelial cell proliferation, and was uncoupled from inflammation because it occurred in mice lacking eosinophils or mast cells, and was independent of macrophage and neutrophil recruitment. CCR3 blockade was more effective at reducing CNV than vascular endothelial growth factor A (VEGF-A) neutralization, which is in clinical use at present, and, unlike VEGF-A blockade, is not toxic to the mouse retina. In vivo imaging with CCR3-targeting quantum dots located spontaneous CNV invisible to standard fluorescein angiography in mice before retinal invasion. CCR3 targeting might reduce vision loss due to AMD through early detection and therapeutic angioinhibition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712122/" 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/PMC2712122/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeda, Atsunobu -- Baffi, Judit Z -- Kleinman, Mark E -- Cho, Won Gil -- Nozaki, Miho -- Yamada, Kiyoshi -- Kaneko, Hiroki -- Albuquerque, Romulo J C -- Dridi, Sami -- Saito, Kuniharu -- Raisler, Brian J -- Budd, Steven J -- Geisen, Pete -- Munitz, Ariel -- Ambati, Balamurali K -- Green, Martha G -- Ishibashi, Tatsuro -- Wright, John D -- Humbles, Alison A -- Gerard, Craig J -- Ogura, Yuichiro -- Pan, Yuzhen -- Smith, Justine R -- Grisanti, Salvatore -- Hartnett, M Elizabeth -- Rothenberg, Marc E -- Ambati, Jayakrishna -- AI039759/AI/NIAID NIH HHS/ -- AI45898/AI/NIAID NIH HHS/ -- DK076893/DK/NIDDK NIH HHS/ -- EY010572/EY/NEI NIH HHS/ -- EY015130/EY/NEI NIH HHS/ -- EY015422/EY/NEI NIH HHS/ -- EY017011/EY/NEI NIH HHS/ -- EY017182/EY/NEI NIH HHS/ -- EY017950/EY/NEI NIH HHS/ -- EY018350/EY/NEI NIH HHS/ -- EY018836/EY/NEI NIH HHS/ -- R01 DK076893/DK/NIDDK NIH HHS/ -- R01 EY015422/EY/NEI NIH HHS/ -- R01 EY015422-04/EY/NEI NIH HHS/ -- R01 EY018350/EY/NEI NIH HHS/ -- R01 EY018350-02/EY/NEI NIH HHS/ -- R01 EY018836/EY/NEI NIH HHS/ -- R01 EY018836-02/EY/NEI NIH HHS/ -- England -- Nature. 2009 Jul 9;460(7252):225-30. doi: 10.1038/nature08151. Epub 2009 Jun 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology & Visual Science, University of Kentucky, Lexington, Kentucky 40506, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19525930" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Movement ; Cell Proliferation ; Cells, Cultured ; Chemokine CCL11/antagonists & inhibitors/metabolism ; Chemokine CCL24/antagonists & inhibitors/metabolism ; Chemokines, CC/antagonists & inhibitors/metabolism ; Choroid/blood supply/cytology/metabolism ; Choroidal Neovascularization/diagnosis/metabolism ; Disease Models, Animal ; Endothelial Cells/cytology/metabolism ; Humans ; Inflammation ; Leukocytes ; Ligands ; Macular Degeneration/*diagnosis/metabolism/*therapy ; Mice ; Mice, Inbred C57BL ; Quantum Dots ; Receptors, CCR3/analysis/*antagonists & ; inhibitors/genetics/immunology/*metabolism ; Retina/drug effects/pathology ; Vascular Endothelial Growth Factor A/antagonists & inhibitors/immunology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    CD8(+) T lymphocyte mobilization to virus-infected tissue requires CD4(+) T-cell help (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-11-10
    Description: CD4(+) T helper cells are well known for their role in providing critical signals during priming of cytotoxic CD8(+) T lymphocyte (CTL) responses in vivo. T-cell help is required for the generation of primary CTL responses as well as in promoting protective CD8(+) memory T-cell development. However, the role of CD4 help in the control of CTL responses at the effector stage is unknown. Here we show that fully helped effector CTLs are themselves not self-sufficient for entry into the infected tissue, but rely on the CD4(+) T cells to provide the necessary cue. CD4(+) T helper cells control the migration of CTL indirectly through the secretion of IFN-gamma and induction of local chemokine secretion in the infected tissue. Our results reveal a previously unappreciated role of CD4 help in mobilizing effector CTL to the peripheral sites of infection where they help to eliminate infected cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789415/" 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/PMC2789415/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakanishi, Yusuke -- Lu, Bao -- Gerard, Craig -- Iwasaki, Akiko -- AI054359/AI/NIAID NIH HHS/ -- AI062428/AI/NIAID NIH HHS/ -- AI39759/AI/NIAID NIH HHS/ -- HL51366/HL/NHLBI NIH HHS/ -- R01 AI054359/AI/NIAID NIH HHS/ -- R01 AI054359-06A2/AI/NIAID NIH HHS/ -- R01 AI062428/AI/NIAID NIH HHS/ -- R01 AI062428-05/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Nov 26;462(7272):510-3. doi: 10.1038/nature08511. Epub 2009 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19898495" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Chemokines/immunology/secretion ; *Chemotaxis ; Female ; Herpes Simplex/immunology/virology ; Herpesvirus 2, Human/*immunology ; Immunity, Mucosal/immunology ; Interferon-gamma/antagonists & inhibitors/immunology/secretion ; Mice ; Mice, Inbred C57BL ; Models, Immunological ; Mucous Membrane/immunology/virology ; Receptors, CXCR3/metabolism ; T-Lymphocytes, Cytotoxic/*cytology/*immunology ; T-Lymphocytes, Helper-Inducer/*immunology/secretion ; Vagina/*immunology/*virology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Regulation of hypoxia-inducible factor 2alpha signaling by the stress-responsive deacetylase sirtuin 1 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: To survive in hostile environments, organisms activate stress-responsive transcriptional regulators that coordinately increase production of protective factors. Hypoxia changes cellular metabolism and thus activates redox-sensitive as well as oxygen-dependent signal transducers. We demonstrate that Sirtuin 1 (Sirt1), a redox-sensing deacetylase, selectively stimulates activity of the transcription factor hypoxia-inducible factor 2 alpha (HIF-2alpha) during hypoxia. The effect of Sirt1 on HIF-2alpha required direct interaction of the proteins and intact deacetylase activity of Sirt1. Select lysine residues in HIF-2alpha that are acetylated during hypoxia confer repression of Sirt1 augmentation by small-molecule inhibitors. In cultured cells and mice, decreasing or increasing Sirt1 activity or levels affected expression of the HIF-2alpha target gene erythropoietin accordingly. Thus, Sirt1 promotes HIF-2 signaling during hypoxia and likely other environmental stresses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dioum, Elhadji M -- Chen, Rui -- Alexander, Matthew S -- Zhang, Quiyang -- Hogg, Richard T -- Gerard, Robert D -- Garcia, Joseph A -- I01 BX000446/BX/BLRD VA/ -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1289-93. doi: 10.1126/science.1169956.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Veterans Affairs North Texas Health Care System, Department of Medicine, 4500 South Lancaster Road, Dallas, TX 75216, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498162" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Amino Acid Substitution ; Animals ; Basic Helix-Loop-Helix Transcription Factors/chemistry/genetics/*metabolism ; *Cell Hypoxia ; Cell Line ; Cell Line, Tumor ; Erythropoietin/genetics ; Gene Expression Regulation ; Humans ; Kidney/metabolism ; Liver/embryology/metabolism ; Mice ; Mice, Knockout ; Mutant Proteins/chemistry/metabolism ; Oxidation-Reduction ; *Signal Transduction ; Sirtuin 1 ; Sirtuins/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Biomedicine. Asthmatics breathe easier when it's SNO-ing (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-06-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerard, Craig -- New York, N.Y. -- Science. 2005 Jun 10;308(5728):1560-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital, Harvard Medical School, Children's Hospital and Harvard Medical School, Boston, MA 02115 USA. craig.gerard@childrens.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15947161" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/pharmacology ; Alcohol Dehydrogenase ; Animals ; Asthma/drug therapy/*physiopathology ; Bronchi/physiology/physiopathology ; Bronchial Hyperreactivity/physiopathology ; Glutathione Reductase/antagonists & inhibitors/genetics/*metabolism ; Humans ; Isoproterenol/pharmacology ; Lung/metabolism/*physiopathology ; Mice ; Mice, Knockout ; Muscle, Smooth/physiology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase Type II ; Receptors, G-Protein-Coupled/metabolism ; S-Nitrosoglutathione/metabolism ; S-Nitrosothiols/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Genome-wide nucleosome specificity and function of chromatin remodellers in ES cells (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-01-28
    Description: ATP-dependent chromatin remodellers allow access to DNA for transcription factors and the general transcription machinery, but whether mammalian chromatin remodellers target specific nucleosomes to regulate transcription is unclear. Here we present genome-wide remodeller-nucleosome interaction profiles for the chromatin remodellers Chd1, Chd2, Chd4, Chd6, Chd8, Chd9, Brg1 and Ep400 in mouse embryonic stem (ES) cells. These remodellers bind one or both full nucleosomes that flank micrococcal nuclease (MNase)-defined nucleosome-free promoter regions (NFRs), where they separate divergent transcription. Surprisingly, large CpG-rich NFRs that extend downstream of annotated transcriptional start sites are nevertheless bound by non-nucleosomal or subnucleosomal histone variants (H3.3 and H2A.Z) and marked by H3K4me3 and H3K27ac modifications. RNA polymerase II therefore navigates hundreds of base pairs of altered chromatin in the sense direction before encountering an MNase-resistant nucleosome at the 3' end of the NFR. Transcriptome analysis after remodeller depletion reveals reciprocal mechanisms of transcriptional regulation by remodellers. Whereas at active genes individual remodellers have either positive or negative roles via altering nucleosome stability, at polycomb-enriched bivalent genes the same remodellers act in an opposite manner. These findings indicate that remodellers target specific nucleosomes at the edge of NFRs, where they regulate ES cell transcriptional programs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Dieuleveult, Maud -- Yen, Kuangyu -- Hmitou, Isabelle -- Depaux, Arnaud -- Boussouar, Faycal -- Dargham, Daria Bou -- Jounier, Sylvie -- Humbertclaude, Helene -- Ribierre, Florence -- Baulard, Celine -- Farrell, Nina P -- Park, Bongsoo -- Keime, Celine -- Carriere, Lucie -- Berlivet, Soizick -- Gut, Marta -- Gut, Ivo -- Werner, Michel -- Deleuze, Jean-Francois -- Olaso, Robert -- Aude, Jean-Christophe -- Chantalat, Sophie -- Pugh, B Franklin -- Gerard, Matthieu -- HG004160/HG/NHGRI NIH HHS/ -- R01 HG004160/HG/NHGRI NIH HHS/ -- England -- Nature. 2016 Feb 4;530(7588):113-6. doi: 10.1038/nature16505. Epub 2016 Jan 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Integrative Biology of the Cell (I2BC), IBITECS, CEA, CNRS, Universite Paris-Sud, Universite Paris-Saclay, 91198 Gif-sur-Yvette, France. ; Key Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases of Guangdong Higher Education Institutes, Department of Developmental Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China. ; Center for Eukaryotic Gene Regulation, Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. ; INSERM, U823; Universite Grenoble Alpes; Institut Albert Bonniot Grenoble, 38700 Grenoble, France. ; Centre National de Genotypage, Institut de Genomique, CEA, 91057 Evry, France. ; IGBMC (Institut de Genetique et de Biologie Moleculaire et Cellulaire), INSERM, U964, CNRS, UMR7104, Universite de Strasbourg, 67404 Illkirch, France. ; Centre Nacional D'Analisi Genomica, 08028 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26814966" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromatin Assembly and Disassembly ; DNA Helicases/metabolism ; DNA-Binding Proteins/*metabolism ; *Gene Expression Regulation ; Genome/*genetics ; Histones/metabolism ; Mice ; Micrococcal Nuclease/metabolism ; Mouse Embryonic Stem Cells/cytology/*metabolism ; Nuclear Proteins/metabolism ; Nucleosomes/*genetics/*metabolism ; Promoter Regions, Genetic/genetics ; RNA Polymerase II/metabolism ; Substrate Specificity ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; Transcription Initiation Site
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Visualization of immediate immune responses to pioneer metastatic cells in the lung (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-03-17
    Description: Lung metastasis is the lethal determinant in many cancers and a number of lines of evidence point to monocytes and macrophages having key roles in its development. Yet little is known about the immediate fate of incoming tumour cells as they colonize this tissue, and even less known about how they make first contact with the immune system. Primary tumours liberate circulating tumour cells (CTCs) into the blood and we have developed a stable intravital two-photon lung imaging model in mice for direct observation of the arrival of CTCs and subsequent host interaction. Here we show dynamic generation of tumour microparticles in shear flow in the capillaries within minutes of CTC entry. Rather than dispersing under flow, many of these microparticles remain attached to the lung vasculature or independently migrate along the inner walls of vessels. Using fluorescent lineage reporters and flow cytometry, we observed 'waves' of distinct myeloid cell subsets that load differentially and sequentially with this CTC-derived material. Many of these tumour-ingesting myeloid cells collectively accumulated in the lung interstitium along with the successful metastatic cells and, as previously understood, promote the development of successful metastases from surviving tumour cells. Although the numbers of these cells rise globally in the lung with metastatic exposure and ingesting myeloid cells undergo phenotypic changes associated with microparticle ingestion, a consistently sparse population of resident conventional dendritic cells, among the last cells to interact with CTCs, confer anti-metastatic protection. This work reveals that CTC fragmentation generates immune-interacting intermediates, and defines a competitive relationship between phagocyte populations for tumour loading during metastatic cell seeding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Headley, Mark B -- Bins, Adriaan -- Nip, Alyssa -- Roberts, Edward W -- Looney, Mark R -- Gerard, Audrey -- Krummel, Matthew F -- P01 HL024136/HL/NHLBI NIH HHS/ -- R21 CA167601/CA/NCI NIH HHS/ -- R21CA167601/CA/NCI NIH HHS/ -- U54 CA163123/CA/NCI NIH HHS/ -- England -- Nature. 2016 Mar 24;531(7595):513-7. doi: 10.1038/nature16985. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of California, San Francisco, 513 Parnassus Ave, HSW512, San Francisco, California 94143-0511, USA. ; Department of Medical Oncology, Academic Medical Center Amsterdam, Meibergdreef, 91105AZ Amsterdam, The Netherlands. ; Departments of Medicine and Laboratory Medicine, University of California, San Francisco, 513 Parnassus Avenue, HSW512, California 94143-0511, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capillaries/pathology ; Cell Line, Tumor ; Cell Lineage ; *Cell Movement ; Dendritic Cells/cytology/immunology ; Female ; Genes, Reporter/genetics ; Humans ; Lung/blood supply/cytology/*immunology/*pathology ; Lung Neoplasms/*immunology/pathology/*secondary ; Male ; Melanoma, Experimental/immunology/pathology ; Mice ; Microscopy, Confocal ; Myeloid Cells/cytology ; Neoplasm Metastasis/*immunology/*pathology ; Neoplastic Cells, Circulating/pathology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...