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  • 1
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    Impaired B and T cell antigen receptor signaling in p110delta PI 3-kinase mutant mice (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-20
    Description: Class IA phosphoinositide 3-kinases (PI3Ks) are a family of p85/p110 heterodimeric lipid kinases that generate second messenger signals downstream of tyrosine kinases, thereby controlling cell metabolism, growth, proliferation, differentiation, motility, and survival. Mammals express three class IA catalytic subunits: p110alpha, p110beta, and p110delta. It is unclear to what extent these p110 isoforms have overlapping or distinct biological roles. Mice expressing a catalytically inactive form of p110delta (p110delta(D910A)) were generated by gene targeting. Antigen receptor signaling in B and T cells was impaired and immune responses in vivo were attenuated in p110delta mutant mice. They also developed inflammatory bowel disease. These results reveal a selective role for p110delta in immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okkenhaug, Klaus -- Bilancio, Antonio -- Farjot, Geraldine -- Priddle, Helen -- Sancho, Sara -- Peskett, Emma -- Pearce, Wayne -- Meek, Stephen E -- Salpekar, Ashreena -- Waterfield, Michael D -- Smith, Andrew J H -- Vanhaesebroeck, Bart -- New York, N.Y. -- Science. 2002 Aug 9;297(5583):1031-4. Epub 2002 Jul 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, 91 Riding House Street, London W1W 7BS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12130661" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; B-Lymphocytes/enzymology/*immunology ; Bone Marrow Cells/cytology ; Catalytic Domain ; Cell Differentiation ; Cell Division ; Female ; Gene Targeting ; Hematopoietic Stem Cells/cytology ; Immunoglobulins/blood ; Inflammatory Bowel Diseases/immunology/pathology ; Interleukin-2/biosynthesis ; Intestinal Mucosa/pathology ; Lymph Nodes/cytology/pathology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Phosphatidylinositol 3-Kinases/genetics/*metabolism ; Point Mutation ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Receptors, Antigen, B-Cell/*metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Signal Transduction ; Spleen/cytology/pathology ; T-Lymphocytes/enzymology/*immunology ; Thymus Gland/cytology
    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)
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  • 2
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    Angiogenesis selectively requires the p110alpha isoform of PI3K to control endothelial cell migration (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-05-02
    Description: Phosphoinositide 3-kinases (PI3Ks) signal downstream of multiple cell-surface receptor types. Class IA PI3K isoforms couple to tyrosine kinases and consist of a p110 catalytic subunit (p110alpha, p110beta or p110delta), constitutively bound to one of five distinct p85 regulatory subunits. PI3Ks have been implicated in angiogenesis, but little is known about potential selectivity among the PI3K isoforms and their mechanism of action in endothelial cells during angiogenesis in vivo. Here we show that only p110alpha activity is essential for vascular development. Ubiquitous or endothelial cell-specific inactivation of p110alpha led to embryonic lethality at mid-gestation because of severe defects in angiogenic sprouting and vascular remodelling. p110alpha exerts this critical endothelial cell-autonomous function by regulating endothelial cell migration through the small GTPase RhoA. p110alpha activity is particularly high in endothelial cells and preferentially induced by tyrosine kinase ligands (such as vascular endothelial growth factor (VEGF)-A). In contrast, p110beta in endothelial cells signals downstream of G-protein-coupled receptor (GPCR) ligands such as SDF-1alpha, whereas p110delta is expressed at low level and contributes only minimally to PI3K activity in endothelial cells. These results provide the first in vivo evidence for p110-isoform selectivity in endothelial PI3K signalling during angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graupera, Mariona -- Guillermet-Guibert, Julie -- Foukas, Lazaros C -- Phng, Li-Kun -- Cain, Robert J -- Salpekar, Ashreena -- Pearce, Wayne -- Meek, Stephen -- Millan, Jaime -- Cutillas, Pedro R -- Smith, Andrew J H -- Ridley, Anne J -- Ruhrberg, Christiana -- Gerhardt, Holger -- Vanhaesebroeck, Bart -- BB/C505659/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/C505659/2/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0601093/Medical Research Council/United Kingdom -- G0601093(79633)/Medical Research Council/United Kingdom -- G0700711/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2008 May 29;453(7195):662-6. doi: 10.1038/nature06892. Epub 2008 Apr 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Cell Signalling, Institute of Cancer, Queen Mary, University of London, Charterhouse Square, London EC1M 6BQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18449193" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Movement ; Cells, Cultured ; Class I Phosphatidylinositol 3-Kinases ; Endothelial Cells/*cytology/*enzymology ; Female ; Humans ; Mice ; *Neovascularization, Physiologic ; Phosphatidylinositol 3-Kinases/genetics/*metabolism ; RNA Interference ; Rats ; Signal Transduction/drug effects ; Vascular Endothelial Growth Factor A/pharmacology ; Wounds and Injuries ; rho GTP-Binding Proteins/metabolism
    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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  • 3
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    Amateur scientists: Citizen projects can minimize conflicts (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearce-Higgins, James W -- England -- Nature. 2015 Sep 24;525(7570):455. doi: 10.1038/525455b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉British Trust for Ornithology, Thetford, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26399822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds ; *Conflict of Interest ; Cost-Benefit Analysis ; Data Collection ; Great Britain ; *Hobbies ; Motivation ; *Research Design ; Science/*manpower ; *Volunteers/psychology
    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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  • 4
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    Inactivation of PI(3)K p110delta breaks regulatory T-cell-mediated immune tolerance to cancer (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-06-12
    Description: Inhibitors against the p110delta isoform of phosphoinositide-3-OH kinase (PI(3)K) have shown remarkable therapeutic efficacy in some human leukaemias. As p110delta is primarily expressed in leukocytes, drugs against p110delta have not been considered for the treatment of solid tumours. Here we report that p110delta inactivation in mice protects against a broad range of cancers, including non-haematological solid tumours. We demonstrate that p110delta inactivation in regulatory T cells unleashes CD8(+) cytotoxic T cells and induces tumour regression. Thus, p110delta inhibitors can break tumour-induced immune tolerance and should be considered for wider use in oncology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4501086/" 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/PMC4501086/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ali, Khaled -- Soond, Dalya R -- Pineiro, Roberto -- Hagemann, Thorsten -- Pearce, Wayne -- Lim, Ee Lyn -- Bouabe, Hicham -- Scudamore, Cheryl L -- Hancox, Timothy -- Maecker, Heather -- Friedman, Lori -- Turner, Martin -- Okkenhaug, Klaus -- Vanhaesebroeck, Bart -- 095691/Wellcome Trust/United Kingdom -- 095691/Z/11/Z/Wellcome Trust/United Kingdom -- 12888/Cancer Research UK/United Kingdom -- 14355/Cancer Research UK/United Kingdom -- A10200/Cancer Research UK/United Kingdom -- A12888/Cancer Research UK/United Kingdom -- A15965/Cancer Research UK/United Kingdom -- BB/E009867/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- C18270/A12888/Cancer Research UK/United Kingdom -- C23338/A10200/Cancer Research UK/United Kingdom -- C23338/A15965/Cancer Research UK/United Kingdom -- England -- Nature. 2014 Jun 19;510(7505):407-11. doi: 10.1038/nature13444. Epub 2014 Jun 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] UCL Cancer Institute, Paul O'Gorman Building, University College London, 72 Huntley Street London WC1E 6DD, UK [2]. ; 1] Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK [2] [3]. ; Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. ; UCL Cancer Institute, Paul O'Gorman Building, University College London, 72 Huntley Street London WC1E 6DD, UK. ; Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK. ; Mary Lyon Centre, MRC Harwell, Harwell Science and Innovation Campus, Harwell OX11 0RD, UK. ; Piramed Pharma, 957 Buckingham Avenue, Slough, Berkshire SL1 4NL, UK. ; Cancer Signaling and Translational Oncology, Genentech Inc, 1 DNA Way, South San Francisco, California 94080-4990, USA. ; 1] Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24919154" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/pharmacology ; Enzyme Activation/drug effects ; Enzyme Inhibitors/*pharmacology ; Immune Tolerance/*drug effects/immunology ; Mice ; Neoplasms/*enzymology/*immunology ; Phosphatidylinositol 3-Kinases/*metabolism ; T-Lymphocytes, Regulatory/*drug effects/enzymology/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)
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