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  • 1
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    Salmonella pathogenicity island 2-dependent evasion of the phagocyte NADPH oxidase (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-04
    Description: A type III protein secretion system encoded by Salmonella pathogenicity island 2 (SPI2) has been found to be required for virulence and survival within macrophages. Here, SPI2 was shown to allow Salmonella typhimurium to avoid NADPH oxidase-dependent killing by macrophages. The ability of SPI2-mutant bacteria to survive in macrophages and to cause lethal infection in mice was restored by abrogation of the NADPH oxidase-dependent respiratory burst. Ultrastructural and immunofluorescence microscopy demonstrated efficient localization of the NADPH oxidase in the proximity of vacuoles containing SPI2-mutant but not wild-type bacteria, suggesting that SPI2 interferes with trafficking of oxidase-containing vesicles to the phagosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vazquez-Torres, A -- Xu, Y -- Jones-Carson, J -- Holden, D W -- Lucia, S M -- Dinauer, M C -- Mastroeni, P -- Fang, F C -- AI39557/AI/NIAID NIH HHS/ -- AI44486/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 3;287(5458):1655-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10698741" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics/physiology ; Cerium/analysis ; Genes, Bacterial ; *Hydroxides ; Macrophages, Peritoneal/*enzymology/*microbiology/ultrastructure ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microscopy, Electron ; Microscopy, Fluorescence ; NADPH Oxidase/*metabolism ; Peroxides/analysis ; Phagosomes/microbiology ; Respiratory Burst ; Salmonella Infections, Animal/microbiology ; Salmonella typhimurium/*genetics/*pathogenicity/physiology ; Superoxides/metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Vacuoles/enzymology/microbiology ; Virulence
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Caveolin-1 is essential for liver regeneration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-16
    Description: Liver regeneration is an orchestrated cellular response that coordinates cell activation, lipid metabolism, and cell division. We found that caveolin-1 gene-disrupted mice (cav1-/- mice) exhibited impaired liver regeneration and low survival after a partial hepatectomy. Hepatocytes showed dramatically reduced lipid droplet accumulation and did not advance through the cell division cycle. Treatment of cav1-/- mice with glucose (which is a predominant energy substrate when compared to lipids) drastically increased survival and reestablished progression of the cell cycle. Thus, caveolin-1 plays a crucial role in the mechanisms that coordinate lipid metabolism with the proliferative response occurring in the liver after cellular injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez, Manuel A -- Albor, Cecilia -- Ingelmo-Torres, Mercedes -- Nixon, Susan J -- Ferguson, Charles -- Kurzchalia, Teymuras -- Tebar, Francesc -- Enrich, Carlos -- Parton, Robert G -- Pol, Albert -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1628-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departament de Biologia Cellular, Facultat de Medicina, Institut d'Investigacions Biomediques August Pi i Sunyer, Universitat de Barcelona, Casanova 143, 08036 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973879" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caveolae/metabolism ; Caveolin 1/genetics/*physiology ; Cell Cycle ; Cell Division ; Fatty Acids/blood/metabolism ; Glucose/administration & dosage ; Hepatectomy ; Hepatocyte Growth Factor/metabolism ; Hepatocytes/cytology/*metabolism ; *Lipid Metabolism ; Lipids/blood ; Liver/metabolism/ultrastructure ; *Liver Regeneration ; Male ; Mice ; Phosphorylation ; RNA, Small Interfering ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Triglycerides/blood/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    CCR5 is a receptor for Staphylococcus aureus leukotoxin ED (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-12-14
    Description: Pore-forming toxins are critical virulence factors for many bacterial pathogens and are central to Staphylococcus aureus-mediated killing of host cells. S. aureus encodes pore-forming bi-component leukotoxins that are toxic towards neutrophils, but also specifically target other immune cells. Despite decades since the first description of staphylococcal leukocidal activity, the host factors responsible for the selectivity of leukotoxins towards different immune cells remain unknown. Here we identify the human immunodeficiency virus (HIV) co-receptor CCR5 as a cellular determinant required for cytotoxic targeting of subsets of myeloid cells and T lymphocytes by the S. aureus leukotoxin ED (LukED). We further demonstrate that LukED-dependent cell killing is blocked by CCR5 receptor antagonists, including the HIV drug maraviroc. Remarkably, CCR5-deficient mice are largely resistant to lethal S. aureus infection, highlighting the importance of CCR5 targeting in S. aureus pathogenesis. Thus, depletion of CCR5(+) leukocytes by LukED suggests a new immune evasion mechanism of S. aureus that can be therapeutically targeted.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536884/" 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/PMC3536884/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alonzo, Francis 3rd -- Kozhaya, Lina -- Rawlings, Stephen A -- Reyes-Robles, Tamara -- DuMont, Ashley L -- Myszka, David G -- Landau, Nathaniel R -- Unutmaz, Derya -- Torres, Victor J -- F32 AI098395/AI/NIAID NIH HHS/ -- R01 AI065303/AI/NIAID NIH HHS/ -- R01-AI065303/AI/NIAID NIH HHS/ -- R21 AI087973/AI/NIAID NIH HHS/ -- R21-AI087973/AI/NIAID NIH HHS/ -- R42-MH084372-02A1/MH/NIMH NIH HHS/ -- R56-AI091856-01A1/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Jan 3;493(7430):51-5. doi: 10.1038/nature11724. Epub 2012 Dec 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23235831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Toxins/*metabolism ; CCR5 Receptor Antagonists ; Cell Death ; Cells, Cultured ; Dendritic Cells/cytology/immunology/metabolism ; Exotoxins/*metabolism ; Female ; Humans ; Immune Evasion ; Immunologic Memory ; Jurkat Cells ; Mice ; Myeloid Cells/cytology/immunology/metabolism ; Receptors, CCR5/*metabolism ; Staphylococcus aureus/immunology/*pathogenicity ; T-Lymphocytes/cytology/immunology/metabolism
    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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    Myc-driven endogenous cell competition in the early mammalian embryo (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-07-12
    Description: The epiblast is the mammalian embryonic tissue that contains the pluripotent stem cells that generate the whole embryo. We have established a method for inducing functional genetic mosaics in the mouse. Using this system, here we show that induction of a mosaic imbalance of Myc expression in the epiblast provokes the expansion of cells with higher Myc levels through the apoptotic elimination of cells with lower levels, without disrupting development. In contrast, homogeneous shifts in Myc levels did not affect epiblast cell viability, indicating that the observed competition results from comparison of relative Myc levels between epiblast cells. During normal development we found that Myc levels are intrinsically heterogeneous among epiblast cells, and that endogenous cell competition refines the epiblast cell population through the elimination of cells with low relative Myc levels. These results show that natural cell competition in the early mammalian embryo contributes to the selection of the epiblast cell pool.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Claveria, Cristina -- Giovinazzo, Giovanna -- Sierra, Rocio -- Torres, Miguel -- England -- Nature. 2013 Aug 1;500(7460):39-44. doi: 10.1038/nature12389. Epub 2013 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departamento de Desarrollo y Reparacion Cardiovascular, Centro Nacional de Investigaciones Cardiovasculares, Madrid E-28029, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23842495" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Proliferation ; Embryo, Mammalian/*cytology/*metabolism ; Embryonic Stem Cells/cytology/metabolism ; Female ; Gene Expression ; Genes, myc ; Germ Layers/*cytology/metabolism ; Male ; Mice ; Models, Biological ; Mosaicism/embryology ; Proto-Oncogene Proteins c-myc/*metabolism
    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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    Focused specificity of intestinal TH17 cells towards commensal bacterial antigens (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-04-18
    Description: T-helper-17 (TH17) cells have critical roles in mucosal defence and in autoimmune disease pathogenesis. They are most abundant in the small intestine lamina propria, where their presence requires colonization of mice with microbiota. Segmented filamentous bacteria (SFB) are sufficient to induce TH17 cells and to promote TH17-dependent autoimmune disease in animal models. However, the specificity of TH17 cells, the mechanism of their induction by distinct bacteria, and the means by which they foster tissue-specific inflammation remain unknown. Here we show that the T-cell antigen receptor (TCR) repertoire of intestinal TH17 cells in SFB-colonized mice has minimal overlap with that of other intestinal CD4(+) T cells and that most TH17 cells, but not other T cells, recognize antigens encoded by SFB. T cells with antigen receptors specific for SFB-encoded peptides differentiated into RORgammat-expressing TH17 cells, even if SFB-colonized mice also harboured a strong TH1 cell inducer, Listeria monocytogenes, in their intestine. The match of T-cell effector function with antigen specificity is thus determined by the type of bacteria that produce the antigen. These findings have significant implications for understanding how commensal microbiota contribute to organ-specific autoimmunity and for developing novel mucosal vaccines.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4128479/" 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/PMC4128479/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Yi -- Torchinsky, Miriam B -- Gobert, Michael -- Xiong, Huizhong -- Xu, Mo -- Linehan, Jonathan L -- Alonzo, Francis -- Ng, Charles -- Chen, Alessandra -- Lin, Xiyao -- Sczesnak, Andrew -- Liao, Jia-Jun -- Torres, Victor J -- Jenkins, Marc K -- Lafaille, Juan J -- Littman, Dan R -- 5P30CA016087-32/CA/NCI NIH HHS/ -- P30 CA077598/CA/NCI NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- UL1 TR00038/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Jun 5;510(7503):152-6. doi: 10.1038/nature13279. Epub 2014 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA. ; 1] Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA [2] Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0485, USA. ; Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA. ; Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA. ; 1] The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA [2] Howard Hughes Medical Institute, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24739972" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/chemistry/*immunology ; Bacterial Vaccines ; Cell Differentiation ; Epitopes, T-Lymphocyte/chemistry/immunology ; Gram-Positive Bacteria/chemistry/*immunology ; Hybridomas/immunology ; Immunity, Mucosal/immunology ; Intestinal Mucosa/cytology/immunology ; Intestine, Small/cytology/immunology ; Intestines/cytology/*immunology ; Listeria monocytogenes/immunology ; Mice ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Receptors, Antigen, T-Cell/immunology ; *Symbiosis ; Th17 Cells/cytology/*immunology
    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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    In vivo discovery of immunotherapy targets in the tumour microenvironment (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-01-31
    Description: Recent clinical trials showed that targeting of inhibitory receptors on T cells induces durable responses in a subset of cancer patients, despite advanced disease. However, the regulatory switches controlling T-cell function in immunosuppressive tumours are not well understood. Here we show that such inhibitory mechanisms can be systematically discovered in the tumour microenvironment. We devised an in vivo pooled short hairpin RNA (shRNA) screen in which shRNAs targeting negative regulators became highly enriched in murine tumours by releasing a block on T-cell proliferation upon tumour antigen recognition. Such shRNAs were identified by deep sequencing of the shRNA cassette from T cells infiltrating tumour or control tissues. One of the target genes was Ppp2r2d, a regulatory subunit of the PP2A phosphatase family. In tumours, Ppp2r2d knockdown inhibited T-cell apoptosis and enhanced T-cell proliferation as well as cytokine production. Key regulators of immune function can therefore be discovered in relevant tissue microenvironments.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4052214/" 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/PMC4052214/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Penghui -- Shaffer, Donald R -- Alvarez Arias, Diana A -- Nakazaki, Yukoh -- Pos, Wouter -- Torres, Alexis J -- Cremasco, Viviana -- Dougan, Stephanie K -- Cowley, Glenn S -- Elpek, Kutlu -- Brogdon, Jennifer -- Lamb, John -- Turley, Shannon J -- Ploegh, Hidde L -- Root, David E -- Love, J Christopher -- Dranoff, Glenn -- Hacohen, Nir -- Cantor, Harvey -- Wucherpfennig, Kai W -- 1R01CA173750/CA/NCI NIH HHS/ -- DP3 DK097681/DK/NIDDK NIH HHS/ -- P01 AI045757/AI/NIAID NIH HHS/ -- P30 CA014051/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R01 CA173750/CA/NCI NIH HHS/ -- T32 AI007386/AI/NIAID NIH HHS/ -- T32 AI07386/AI/NIAID NIH HHS/ -- England -- Nature. 2014 Feb 6;506(7486):52-7. doi: 10.1038/nature12988. Epub 2014 Jan 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2]. ; 1] Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] [3] Jounce Therapeutics, Cambridge, Massachusetts 02138, USA. ; Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA. ; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA. ; Whitehead Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA. ; Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA. ; 1] Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Jounce Therapeutics, Cambridge, Massachusetts 02138, USA. ; Novartis Institutes for Biomedical Research, Cambridge, Massachusetts 02139, USA. ; Genomics Institute of the Novartis Research Foundation, San Diego, California 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24476824" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/immunology ; Apoptosis/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/cytology/immunology/secretion ; Cell Proliferation ; Cytokines/immunology/secretion ; Female ; Gene Knockdown Techniques ; High-Throughput Nucleotide Sequencing ; *Immunotherapy/methods ; Lymphocytes, Tumor-Infiltrating/cytology/immunology/metabolism/secretion ; Melanoma, Experimental/immunology ; Mice ; Mice, Inbred C57BL ; *Molecular Targeted Therapy ; Protein Phosphatase 2/deficiency/genetics/*metabolism ; RNA, Small Interfering/genetics ; Reproducibility of Results ; Tumor Microenvironment/*immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Control of ground-state pluripotency by allelic regulation of Nanog (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-02-14
    Description: Pluripotency is established through genome-wide reprogramming during mammalian pre-implantation development, resulting in the formation of the naive epiblast. Reprogramming involves both the resetting of epigenetic marks and the activation of pluripotent-cell-specific genes such as Nanog and Oct4 (also known as Pou5f1). The tight regulation of these genes is crucial for reprogramming, but the mechanisms that regulate their expression in vivo have not been uncovered. Here we show that Nanog--but not Oct4--is monoallelically expressed in early pre-implantation embryos. Nanog then undergoes a progressive switch to biallelic expression during the transition towards ground-state pluripotency in the naive epiblast of the late blastocyst. Embryonic stem (ES) cells grown in leukaemia inhibitory factor (LIF) and serum express Nanog mainly monoallelically and show asynchronous replication of the Nanog locus, a feature of monoallelically expressed genes, but ES cells activate both alleles when cultured under 2i conditions, which mimic the pluripotent ground state in vitro. Live-cell imaging with reporter ES cells confirmed the allelic expression of Nanog and revealed allelic switching. The allelic expression of Nanog is regulated through the fibroblast growth factor-extracellular signal-regulated kinase signalling pathway, and it is accompanied by chromatin changes at the proximal promoter but occurs independently of DNA methylation. Nanog-heterozygous blastocysts have fewer inner-cell-mass derivatives and delayed primitive endoderm formation, indicating a role for the biallelic expression of Nanog in the timely maturation of the inner cell mass into a fully reprogrammed pluripotent epiblast. We suggest that the tight regulation of Nanog dose at the chromosome level is necessary for the acquisition of ground-state pluripotency during development. Our data highlight an unexpected role for allelic expression in controlling the dose of pluripotency factors in vivo, adding an extra level to the regulation of reprogramming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyanari, Yusuke -- Torres-Padilla, Maria-Elena -- England -- Nature. 2012 Feb 12;483(7390):470-3. doi: 10.1038/nature10807.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM U964, Universite de Strasbourg, F-67404 Illkirch, Cite Universitaire de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22327294" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Blastocyst/cytology/*metabolism ; Blastocyst Inner Cell Mass/cytology/metabolism ; Cell Cycle Proteins/metabolism ; Cellular Reprogramming/*genetics ; Chromosomal Proteins, Non-Histone/metabolism ; DNA Replication ; Embryonic Stem Cells/drug effects/metabolism ; Female ; *Gene Expression Regulation, Developmental ; Genomic Imprinting ; Germ Layers/cytology/metabolism ; Homeodomain Proteins/*genetics/*metabolism ; In Situ Hybridization, Fluorescence ; Leukemia Inhibitory Factor/pharmacology ; Male ; Mediator Complex/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Octamer Transcription Factor-3 ; Pluripotent Stem Cells/cytology/*metabolism ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Aberrant B cell development and immune response in mice with a compromised BCR complex (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-06-21
    Description: The immunoglobulin alpha (Ig-alpha)-Ig-beta heterodimer is the signaling component of the antigen receptor complex on B cells (BCR) and B cell progenitors (pre-BCR). A mouse mutant that lacks most of the Ig-alpha cytoplasmic tail exhibits only a small impairment in early B cell development but a severe block in the generation of the peripheral B cell pool, revealing a checkpoint in B cell maturation that ensures the expression of a functional BCR on mature B cells. B cells that do develop demonstrate a differential dependence on Ig-alpha signaling in antibody responses such that a signaling-competent Ig-alpha appears to be critical for the response to T-independent, but not T-dependent, antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Torres, R M -- Flaswinkel, H -- Reth, M -- Rajewsky, K -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1804-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650582" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Formation ; Antigens/immunology ; Antigens, CD/chemistry/immunology/*physiology ; Antigens, CD79 ; Antigens, T-Independent/immunology ; B-Lymphocytes/*cytology/*immunology ; Bone Marrow Cells ; Cell Lineage ; Gene Rearrangement, B-Lymphocyte ; Gene Targeting ; Genes, Immunoglobulin ; Hematopoietic Stem Cells/cytology/immunology ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, B-Cell/chemistry/immunology/*physiology ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Metal chelation and inhibition of bacterial growth in tissue abscesses (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-02-16
    Description: Bacterial infection often results in the formation of tissue abscesses, which represent the primary site of interaction between invading bacteria and the innate immune system. We identify the host protein calprotectin as a neutrophil-dependent factor expressed inside Staphylococcus aureus abscesses. Neutrophil-derived calprotectin inhibited S. aureus growth through chelation of nutrient Mn2+ and Zn2+: an activity that results in reprogramming of the bacterial transcriptome. The abscesses of mice lacking calprotectin were enriched in metal, and staphylococcal proliferation was enhanced in these metal-rich abscesses. These results demonstrate that calprotectin is a critical factor in the innate immune response to infection and define metal chelation as a strategy for inhibiting microbial growth inside abscessed tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corbin, Brian D -- Seeley, Erin H -- Raab, Andrea -- Feldmann, Joerg -- Miller, Michael R -- Torres, Victor J -- Anderson, Kelsi L -- Dattilo, Brian M -- Dunman, Paul M -- Gerads, Russell -- Caprioli, Richard M -- Nacken, Wolfgang -- Chazin, Walter J -- Skaar, Eric P -- 5R01 GM58008-09/GM/NIGMS NIH HHS/ -- F32 AI071487/AI/NIAID NIH HHS/ -- P50 CA068485/CA/NCI NIH HHS/ -- R01 GM62112/GM/NIGMS NIH HHS/ -- T32 GM008320/GM/NIGMS NIH HHS/ -- T32 GM08320/GM/NIGMS NIH HHS/ -- T32 HL069765/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2008 Feb 15;319(5865):962-5. doi: 10.1126/science.1152449.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276893" target="_blank"〉PubMed〈/a〉
    Keywords: Abscess/immunology/metabolism/*microbiology ; Animals ; Calcium/metabolism ; Chelating Agents/*metabolism/pharmacology ; Dimerization ; Gene Expression Profiling ; Kidney Diseases/immunology/metabolism/microbiology ; Leukocyte L1 Antigen Complex/genetics/*metabolism/pharmacology ; Liver Abscess/metabolism/microbiology/pathology ; Manganese/*metabolism ; Mass Spectrometry ; Mice ; Neutrophils/*metabolism ; Staphylococcal Infections/immunology/metabolism/*microbiology ; Staphylococcus aureus/drug effects/genetics/*growth & development ; Zinc/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Biomaterials. Electronic dura mater for long-term multimodal neural interfaces (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-01-13
    Description: The mechanical mismatch between soft neural tissues and stiff neural implants hinders the long-term performance of implantable neuroprostheses. Here, we designed and fabricated soft neural implants with the shape and elasticity of dura mater, the protective membrane of the brain and spinal cord. The electronic dura mater, which we call e-dura, embeds interconnects, electrodes, and chemotrodes that sustain millions of mechanical stretch cycles, electrical stimulation pulses, and chemical injections. These integrated modalities enable multiple neuroprosthetic applications. The soft implants extracted cortical states in freely behaving animals for brain-machine interface and delivered electrochemical spinal neuromodulation that restored locomotion after paralyzing spinal cord injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minev, Ivan R -- Musienko, Pavel -- Hirsch, Arthur -- Barraud, Quentin -- Wenger, Nikolaus -- Moraud, Eduardo Martin -- Gandar, Jerome -- Capogrosso, Marco -- Milekovic, Tomislav -- Asboth, Leonie -- Torres, Rafael Fajardo -- Vachicouras, Nicolas -- Liu, Qihan -- Pavlova, Natalia -- Duis, Simone -- Larmagnac, Alexandre -- Voros, Janos -- Micera, Silvestro -- Suo, Zhigang -- Courtine, Gregoire -- Lacour, Stephanie P -- New York, N.Y. -- Science. 2015 Jan 9;347(6218):159-63. doi: 10.1126/science.1260318.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bertarelli Foundation Chair in Neuroprosthetic Technology, Laboratory for Soft Bioelectronic Interfaces, Centre for Neuroprosthetics, Institute of Microengineering and Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne (EPFL), Switzerland. ; International Paraplegic Foundation Chair in Spinal Cord Repair, Centre for Neuroprosthetics and Brain Mind Institute, EPFL, Switzerland. Pavlov Institute of Physiology, St. Petersburg, Russia. ; International Paraplegic Foundation Chair in Spinal Cord Repair, Centre for Neuroprosthetics and Brain Mind Institute, EPFL, Switzerland. ; Translational Neural Engineering Laboratory, Center for Neuroprosthetics and Institute of Bioengineering, EPFL, Lausanne, Switzerland. ; Bertarelli Foundation Chair in Neuroprosthetic Technology, Laboratory for Soft Bioelectronic Interfaces, Centre for Neuroprosthetics, Institute of Microengineering and Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne (EPFL), Switzerland. International Paraplegic Foundation Chair in Spinal Cord Repair, Centre for Neuroprosthetics and Brain Mind Institute, EPFL, Switzerland. ; School of Engineering and Applied Sciences, Kavli Institute for Bionano Science and Technology, Harvard University, Cambridge, MA, USA. ; Laboratory for Biosensors and Bioelectronics, Institute for Biomedical Engineering, University and ETH Zurich, Switzerland. ; Translational Neural Engineering Laboratory, Center for Neuroprosthetics and Institute of Bioengineering, EPFL, Lausanne, Switzerland. The BioRobotics Institute, Scuola Superiore Sant'Anna, Pisa 56025, Italy. ; International Paraplegic Foundation Chair in Spinal Cord Repair, Centre for Neuroprosthetics and Brain Mind Institute, EPFL, Switzerland. gregoire.courtine@epfl.ch stephanie.lacour@epfl.ch. ; Bertarelli Foundation Chair in Neuroprosthetic Technology, Laboratory for Soft Bioelectronic Interfaces, Centre for Neuroprosthetics, Institute of Microengineering and Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne (EPFL), Switzerland. gregoire.courtine@epfl.ch stephanie.lacour@epfl.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25574019" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biocompatible Materials/therapeutic use ; Brain-Computer Interfaces ; Drug Delivery Systems/*methods ; *Dura Mater ; Elasticity ; Electric Stimulation/*methods ; Electrochemotherapy/*methods ; *Electrodes, Implanted ; Locomotion ; Mice ; Mice, Inbred Strains ; Motor Cortex/physiopathology ; Multimodal Imaging ; Neurons/physiology ; Paralysis/etiology/physiopathology/*therapy ; Platinum ; *Prostheses and Implants ; Silicon ; Spinal Cord/physiopathology ; Spinal Cord Injuries/complications/physiopathology/*therapy
    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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