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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brenner, S -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2173-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Sciences Institute, Berkeley, CA 94704, USA. brenner@molsci.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10744539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Computational Biology ; Drosophila melanogaster/genetics ; *Gene Expression Regulation ; Genes ; *Genome ; *Molecular Biology ; *Proteins/chemistry/genetics/physiology ; Sequence Analysis, DNA
    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
    Publication Date: 2000-07-06
    Description: Most developing thymocytes undergo apoptosis because they cannot interact productively with molecules encoded by the major histocompatibility complex. Here, we show that mice lacking the orphan nuclear hormone receptor RORgamma lose thymic expression of the anti-apoptotic factor Bcl-xL. RORgamma thus regulates the survival of CD4+8+ thymocytes and may control the temporal window during which thymocytes can undergo positive selection. RORgamma was also required for development of lymph nodes and Peyer's patches, but not splenic follicles. In its absence, there was loss of a population of CD3-CD4+CD45+ cells that normally express RORgamma and that are likely early progenitors of lymphoid organs. Hence, RORgamma has critical functions in T cell repertoire selection and lymphoid organogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Z -- Unutmaz, D -- Zou, Y R -- Sunshine, M J -- Pierani, A -- Brenner-Morton, S -- Mebius, R E -- Littman, D R -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine and Howard Hughes Medical Institute, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10875923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; *CDC2-CDC28 Kinases ; Cell Count ; Cell Cycle ; Cell Survival ; Crosses, Genetic ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Female ; Gene Targeting ; Inhibitor of Differentiation Protein 2 ; Lymphoid Tissue/cytology/embryology/*growth & development ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics/*physiology ; *Receptors, Retinoic Acid ; *Receptors, Thyroid Hormone ; *Repressor Proteins ; T-Lymphocyte Subsets/*cytology ; Thymus Gland/*cytology ; *Transcription Factors ; bcl-X Protein
    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
    Publication Date: 2002-03-23
    Description: To examine the role of T cell receptor (TCR) in gammadelta T cells in adaptive immunity, a macaque model was used to follow Vgamma2Vdelta2+ T cell responses to mycobacterial infections. These phosphoantigen-specific gammadelta T cells displayed major expansion during Mycobacterium bovis Bacille Calmette-Guerin (BCG) infection and a clear memory-type response after BCG reinfection. Primary and recall expansions of Vgamma2Vdelta2+ T cells were also seen during Mycobacterium tuberculosis infection of naive and BCG-vaccinated macaques, respectively. This capacity to rapidly expand coincided with a clearance of BCG bacteremia and immunity to fatal tuberculosis in BCG-vaccinated macaques. Thus, Vgamma2Vdelta2+ T cells may contribute to adaptive immunity to mycobacterial infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872146/" 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/PMC2872146/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Yun -- Zhou, Dejiang -- Qiu, Liyou -- Lai, Xioamin -- Simon, Meredith -- Shen, Ling -- Kou, Zhongchen -- Wang, Qifan -- Jiang, Liming -- Estep, Jim -- Hunt, Robert -- Clagett, Michelle -- Sehgal, Prabhat K -- Li, Yunyaun -- Zeng, Xuejun -- Morita, Craig T -- Brenner, Michael B -- Letvin, Norman L -- Chen, Zheng W -- HL64560/HL/NHLBI NIH HHS/ -- R01 HL064560/HL/NHLBI NIH HHS/ -- R01 HL064560-04/HL/NHLBI NIH HHS/ -- R01 RR013601/RR/NCRR NIH HHS/ -- R01 RR013601-04/RR/NCRR NIH HHS/ -- RR13601/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2002 Mar 22;295(5563):2255-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tuberculosis Research Unit, Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11910108" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Immunity, Innate/immunology ; Immunologic Memory/immunology ; Lymphocyte Activation ; Lymphocyte Count ; Macaca/*immunology/*microbiology ; Mycobacterium bovis/*immunology ; Mycobacterium tuberculosis/*immunology ; Receptors, Antigen, T-Cell, gamma-delta/*immunology ; T-Lymphocytes/cytology/*immunology ; Tuberculosis/*immunology/microbiology
    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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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryder, O A -- McLaren, A -- Brenner, S -- Zhang, Y P -- Benirschke, K -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):275-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Reproduction of Endangered Species, Zoological Society of San Diego, CA 92112-0551, USA. oryder@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10777408" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Biological Specimen Banks/economics ; *Conservation of Natural Resources ; Costs and Cost Analysis ; *Dna ; Databases, Factual ; *Ecosystem ; Genetic Variation ; *Genome ; Internet ; Registries
    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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  • 5
    Publication Date: 2002-09-07
    Description: Previous studies have revealed that autoantibodies, complement components, and Fc receptors each participate in the pathogenesis of erosive arthritis in K/BxN mice. However, it is not known which cellular populations are responsive to these inflammatory signals. We find that two strains of mice deficient in mast cells, W/Wv and Sl/Sld, were resistant to development of joint inflammation and that susceptibility was restored in the W/Wv strain by mast cell engraftment. Thus, mast cells may function as a cellular link between autoantibodies, soluble mediators, and other effector populations in inflammatory arthritis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, David M -- Friend, Daniel S -- Gurish, Michael F -- Benoist, Christophe -- Mathis, Diane -- Brenner, Michael B -- 1R01 AR/AI46580-01/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Sep 6;297(5587):1689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12215644" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/*immunology/pathology ; Autoantibodies/*immunology ; Blood Transfusion ; Bone Marrow Transplantation ; Cell Degranulation ; Joints/*immunology/pathology ; Male ; Mast Cells/*immunology/transplantation ; Mice ; Mice, Inbred C57BL
    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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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-09-02
    Description: Many of the intricate pathways of apoptosis that instruct a cell to kill itself involve the convergence of key proteins on the membranes of mitochondria. Such proteins induce the permeabilization of mitochondrial membranes and the release of caspase enzymes and nuclease activators that set in motion the final stages of programmed cell death. Now, as Brenner and Kroemer discuss in their Perspective, a proapoptotic transcription factor called TR3 has been found to move from its normal location in the nucleus to the mitochondria and to promote release of cytochrome c, a key event in apoptosis (Li et al.)〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brenner, C -- Kroemer, G -- New York, N.Y. -- Science. 2000 Aug 18;289(5482):1150-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Apoptosis, Cancer and Immunity Laboratory, National League Against Cancer, CNRS-UMR1599, Institut Gustave Roussy, F-94805 Villejuif, France. catherine.brenner@utc.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10970229" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Nucleus/metabolism ; Cytochrome c Group/metabolism ; DNA/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Gene Expression Regulation ; Humans ; Intracellular Membranes/*metabolism/physiology ; Mice ; Mice, Transgenic ; Mitochondria/*metabolism ; Nerve Growth Factor/pharmacology ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Permeability ; Protein Structure, Tertiary ; Receptors, Cytoplasmic and Nuclear ; Receptors, Steroid ; Response Elements ; Signal Transduction ; T-Lymphocytes/cytology/immunology ; Transcription Factors/chemistry/genetics/*metabolism ; Zinc Fingers
    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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  • 7
    Publication Date: 1998-09-25
    Description: The proapoptotic Bax protein induces cell death by acting on mitochondria. Bax binds to the permeability transition pore complex (PTPC), a composite proteaceous channel that is involved in the regulation of mitochondrial membrane permeability. Immunodepletion of Bax from PTPC or purification of PTPC from Bax-deficient mice yielded a PTPC that could not permeabilize membranes in response to atractyloside, a proapoptotic ligand of the adenine nucleotide translocator (ANT). Bax and ANT coimmunoprecipitated and interacted in the yeast two-hybrid system. Ectopic expression of Bax induced cell death in wild-type but not in ANT-deficient yeast. Recombinant Bax and purified ANT, but neither of them alone, efficiently formed atractyloside-responsive channels in artificial membranes. Hence, the proapoptotic molecule Bax and the constitutive mitochondrial protein ANT cooperate within the PTPC to increase mitochondrial membrane permeability and to trigger cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marzo, I -- Brenner, C -- Zamzami, N -- Jurgensmeier, J M -- Susin, S A -- Vieira, H L -- Prevost, M C -- Xie, Z -- Matsuyama, S -- Reed, J C -- Kroemer, G -- New York, N.Y. -- Science. 1998 Sep 25;281(5385):2027-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS, UPR 420, 19 rue Guy Moquet, F-94801 Villejuif, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9748162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Atractyloside/metabolism/pharmacology ; Binding Sites ; Bongkrekic Acid/metabolism/pharmacology ; Cyclosporine/pharmacology ; Dimerization ; HT29 Cells ; Humans ; Intracellular Membranes/physiology ; Liposomes ; Mice ; Mice, Inbred C57BL ; Mitochondria/*physiology ; Mitochondrial ADP, ATP Translocases/chemistry/*metabolism ; Permeability ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism/pharmacology ; Proto-Oncogene Proteins c-bcl-2/pharmacology ; Rats ; Rats, Wistar ; Recombinant Proteins/pharmacology ; Saccharomyces cerevisiae/cytology/genetics ; Transfection ; bcl-2-Associated X Protein
    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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  • 8
    Publication Date: 2008-01-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, David -- Brenner, Sydney -- England -- Nature. 2008 Jan 10;451(7175):139. doi: 10.1038/451139a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉David Anderson is in the Division of Biology, 216-276 Howard Hughes Medical Institute, California Institute of Technology, Pasadena, California 91125, USA.wuwei@caltech.edu; sbrenner@salk.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18185579" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics ; Animals ; Drosophila melanogaster/genetics/physiology ; History, 20th Century ; History, 21st Century ; Molecular Biology/*history ; Neurobiology/history
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2015-08-14
    Description: Coleoid cephalopods (octopus, squid and cuttlefish) are active, resourceful predators with a rich behavioural repertoire. They have the largest nervous systems among the invertebrates and present other striking morphological innovations including camera-like eyes, prehensile arms, a highly derived early embryogenesis and a remarkably sophisticated adaptive colouration system. To investigate the molecular bases of cephalopod brain and body innovations, we sequenced the genome and multiple transcriptomes of the California two-spot octopus, Octopus bimaculoides. We found no evidence for hypothesized whole-genome duplications in the octopus lineage. The core developmental and neuronal gene repertoire of the octopus is broadly similar to that found across invertebrate bilaterians, except for massive expansions in two gene families previously thought to be uniquely enlarged in vertebrates: the protocadherins, which regulate neuronal development, and the C2H2 superfamily of zinc-finger transcription factors. Extensive messenger RNA editing generates transcript and protein diversity in genes involved in neural excitability, as previously described, as well as in genes participating in a broad range of other cellular functions. We identified hundreds of cephalopod-specific genes, many of which showed elevated expression levels in such specialized structures as the skin, the suckers and the nervous system. Finally, we found evidence for large-scale genomic rearrangements that are closely associated with transposable element expansions. Our analysis suggests that substantial expansion of a handful of gene families, along with extensive remodelling of genome linkage and repetitive content, played a critical role in the evolution of cephalopod morphological innovations, including their large and complex nervous systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Albertin, Caroline B -- Simakov, Oleg -- Mitros, Therese -- Wang, Z Yan -- Pungor, Judit R -- Edsinger-Gonzales, Eric -- Brenner, Sydney -- Ragsdale, Clifton W -- Rokhsar, Daniel S -- R03 HD056094/HD/NICHD NIH HHS/ -- R03HD064887/HD/NICHD NIH HHS/ -- S10RR027303/RR/NCRR NIH HHS/ -- S10RR029668/RR/NCRR NIH HHS/ -- T32 HD055164/HD/NICHD NIH HHS/ -- UL1 TR000430/TR/NCATS NIH HHS/ -- England -- Nature. 2015 Aug 13;524(7564):220-4. doi: 10.1038/nature14668.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Organismal Biology and Anatomy, University of Chicago, Chicago, Illinois 60637, USA. ; 1] Okinawa Institute of Science and Technology Graduate University, Onna, Okinawa 9040495, Japan [2] Centre for Organismal Studies, University of Heidelberg, 69117 Heidelberg, Germany. ; Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA. ; Department of Neurobiology, University of Chicago, Chicago, Illinois 60637, USA. ; 1] Okinawa Institute of Science and Technology Graduate University, Onna, Okinawa 9040495, Japan [2] Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA. ; Okinawa Institute of Science and Technology Graduate University, Onna, Okinawa 9040495, Japan. ; 1] Department of Organismal Biology and Anatomy, University of Chicago, Chicago, Illinois 60637, USA [2] Department of Neurobiology, University of Chicago, Chicago, Illinois 60637, USA. ; 1] Okinawa Institute of Science and Technology Graduate University, Onna, Okinawa 9040495, Japan [2] Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA [3] 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/26268193" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Structures/*anatomy & histology/*metabolism ; Animals ; Cadherins/genetics ; DNA Copy Number Variations/genetics ; DNA Transposable Elements/genetics ; Decapodiformes/genetics ; *Evolution, Molecular ; Genome/*genetics ; Genomics ; Ion Channels/genetics/metabolism ; Nervous System/*anatomy & histology/metabolism ; Octopodiformes/*anatomy & histology/classification/*genetics ; Organ Specificity ; Phylogeny ; RNA Editing/genetics ; RNA, Messenger/genetics/metabolism ; Species Specificity ; Transcription Factors/genetics ; Zinc Fingers
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1992-02-21
    Description: A class of regulators of eukaryotic gene expression contains a conserved amino acid sequence responsible for protein oligomerization and binding to DNA. This structure consists of an arginine- and lysine-rich basic region followed by a helix-loop-helix motif, which together mediate specific binding to DNA. Peptides were prepared that span this motif in the MyoD protein; in solution, they formed alpha-helical dimers and tetramers. They bound to DNA as dimers and their alpha-helical content increased on binding. Parallel and antiparallel four-helix models of the DNA-bound dimer were constructed. Peptides containing disulfide bonds were engineered to test the correctness of the two models. A disulfide that is compatible with the parallel model promotes specific interaction with DNA, whereas a disulfide compatible with the antiparallel model abolishes specific binding. Electron paramagnetic resonance (EPR) measurements of nitroxide-labeled peptides provided intersubunit distance measurements that also supported the parallel model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anthony-Cahill, S J -- Benfield, P A -- Fairman, R -- Wasserman, Z R -- Brenner, S L -- Stafford, W F 3rd -- Altenbach, C -- Hubbell, W L -- DeGrado, W F -- GM13731/GM/NIGMS NIH HHS/ -- GM14321/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 21;255(5047):979-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotechnology Department, DuPont Merck Pharmaceutical Co., Wilmington, DE 19880-0328.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1312255" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Circular Dichroism ; DNA-Binding Proteins/*chemistry ; Disulfides ; Electron Spin Resonance Spectroscopy ; Enhancer Elements, Genetic ; Gene Expression Regulation ; Humans ; Models, Molecular ; Molecular Sequence Data ; Protein Conformation ; Regulatory Sequences, Nucleic Acid ; Sequence Alignment ; Transcription Factors/*chemistry
    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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