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
Filter
  • Articles  (14)
  • Data
  • Cell Line  (14)
  • 2000-2004  (14)
  • 1975-1979
  • 2004  (14)
Collection
  • Articles  (14)
  • Data
Source
Keywords
Publisher
Years
  • 2000-2004  (14)
  • 1975-1979
Year
Journal
Topic
  • 1
    facet.materialart.
    Unknown
    Zebrafish Dpr2 inhibits mesoderm induction by promoting degradation of nodal receptors (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-02
    Description: Nodal proteins, members of the transforming growth factor-beta (TGFbeta) superfamily, have been identified as key endogenous mesoderm inducers in vertebrates. Precise control of Nodal signaling is essential for normal development of embryos. Here, we report that zebrafish dapper2 (dpr2) is expressed in mesoderm precursors during early embryogenesis and is positively regulated by Nodal signals. In vivo functional studies in zebrafish suggest that Dpr2 suppresses mesoderm induction activities of Nodal signaling. Dpr2 is localized in late endosomes, binds to the TGFbeta receptors ALK5 and ALK4, and accelerates lysosomal degradation of these receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Lixia -- Zhou, Hu -- Su, Ying -- Sun, Zhihui -- Zhang, Haiwen -- Zhang, Long -- Zhang, Yu -- Ning, Yuanheng -- Chen, Ye-Guang -- Meng, Anming -- New York, N.Y. -- Science. 2004 Oct 1;306(5693):114-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Biology, Ministry of Education (MOE), Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing 100084, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15459392" target="_blank"〉PubMed〈/a〉
    Keywords: Activin Receptors, Type I/*metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; Embryo, Nonmammalian/embryology/*metabolism ; *Embryonic Induction ; Endosomes/metabolism ; Fluorescent Antibody Technique ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Humans ; In Situ Hybridization ; Intracellular Signaling Peptides and Proteins ; Lysosomes/metabolism ; Mesoderm/*physiology ; Molecular Sequence Data ; Mutation ; Nodal Signaling Ligands ; Oligonucleotides, Antisense ; Protein-Serine-Threonine Kinases ; Proteins/metabolism ; Receptors, Transforming Growth Factor beta/*metabolism ; Signal Transduction ; Transforming Growth Factor beta/genetics/metabolism ; Zebrafish/*embryology/genetics/metabolism ; Zebrafish Proteins/chemistry/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
  • 2
    facet.materialart.
    Unknown
    Lysosomal glycosphingolipid recognition by NKT cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-13
    Description: NKT cells represent a distinct lineage of T cells that coexpress a conserved alphabeta T cell receptor (TCR) and natural killer (NK) receptors. Although the TCR of NKT cells is characteristically autoreactive to CD1d, a lipid-presenting molecule, endogenous ligands for these cells have not been identified. We show that a lysosomal glycosphingolipid of previously unknown function, isoglobotrihexosylceramide (iGb3), is recognized both by mouse and human NKT cells. Impaired generation of lysosomal iGb3 in mice lacking beta-hexosaminidase b results in severe NKT cell deficiency, suggesting that this lipid also mediates development of NKT cells in the mouse. We suggest that expression of iGb3 in peripheral tissues may be involved in controlling NKT cell responses to infections and malignancy and in autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Dapeng -- Mattner, Jochen -- Cantu, Carlos 3rd -- Schrantz, Nicolas -- Yin, Ning -- Gao, Ying -- Sagiv, Yuval -- Hudspeth, Kelly -- Wu, Yun-Ping -- Yamashita, Tadashi -- Teneberg, Susann -- Wang, Dacheng -- Proia, Richard L -- Levery, Steven B -- Savage, Paul B -- Teyton, Luc -- Bendelac, Albert -- AI053725/AI/NIAID NIH HHS/ -- AI50847/AI/NIAID NIH HHS/ -- P20RR16459/RR/NCRR NIH HHS/ -- R01 AI38339/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 3;306(5702):1786-9. Epub 2004 Nov 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Chicago, Department of Pathology, Chicago, IL 60637, USA. dzhou@midway.uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15539565" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens, CD1/immunology/metabolism ; Antigens, CD1d ; Autoimmunity ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Dendritic Cells/immunology ; Galactosyltransferases/genetics/metabolism ; Globosides/chemistry/*immunology/metabolism ; Humans ; Hybridomas ; Infection/immunology ; Killer Cells, Natural/*immunology ; Ligands ; Lymphocyte Activation ; Lymphocyte Count ; Lysosomes/*metabolism ; Mice ; Mice, Inbred C57BL ; Neoplasms/immunology ; Plant Lectins/immunology ; Rats ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Saposins/metabolism ; T-Lymphocyte Subsets/*immunology ; beta-N-Acetylhexosaminidases/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
  • 3
    facet.materialart.
    Unknown
    Use of CD134 as a primary receptor by the feline immunodeficiency virus (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-21
    Description: Feline immunodeficiency virus (FIV) induces a disease similar to acquired immunodeficiency syndrome (AIDS) in cats, yet in contrast to human immunodeficiency virus (HIV), CD4 is not the viral receptor. We identified a primary receptor for FIV as CD134 (OX40), a T cell activation antigen and costimulatory molecule. CD134 expression promotes viral binding and renders cells permissive for viral entry, productive infection, and syncytium formation. Infection is CXCR4-dependent, analogous to infection with X4 strains of HIV. Thus, despite the evolutionary divergence of the feline and human lentiviruses, both viruses use receptors that target the virus to a subset of cells that are pivotal to the acquired immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimojima, Masayuki -- Miyazawa, Takayuki -- Ikeda, Yasuhiro -- McMonagle, Elizabeth L -- Haining, Hayley -- Akashi, Hiroomi -- Takeuchi, Yasuhiro -- Hosie, Margaret J -- Willett, Brian J -- R01 AI49765-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 20;303(5661):1192-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterinary Microbiology, Graduate School of Agricultural and Life Sciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14976315" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; CD4-Positive T-Lymphocytes/immunology/metabolism/virology ; Cats ; Cell Line ; Cell Line, Tumor ; DNA, Complementary ; Gene Library ; HIV/metabolism ; HeLa Cells ; Heterocyclic Compounds/pharmacology ; Humans ; Immunodeficiency Virus, Feline/*metabolism/pathogenicity ; Mice ; Molecular Sequence Data ; NIH 3T3 Cells ; Receptors, CXCR4/antagonists & inhibitors/metabolism ; Receptors, OX40 ; Receptors, Tumor Necrosis Factor/chemistry/genetics/immunology/*metabolism ; Receptors, Virus/chemistry/genetics/immunology/*metabolism ; Species Specificity ; Transduction, Genetic ; Transfection
    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
    RAD51C is required for Holliday junction processing in mammalian cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-13
    Description: During genetic recombination and the recombinational repair of chromosome breaks, DNA molecules become linked at points of strand exchange. Branch migration and resolution of these crossovers, or Holliday junctions (HJs), complete the recombination process. Here, we show that extracts from cells carrying mutations in the recombination/repair genes RAD51C or XRCC3 have reduced levels of HJ resolvase activity. Moreover, depletion of RAD51C from fractionated human extracts caused a loss of branch migration and resolution activity, but these functions were restored by complementation with a variety of RAD51 paralog complexes containing RAD51C. We conclude that the RAD51 paralogs are involved in HJ processing in human cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Yilun -- Masson, Jean-Yves -- Shah, Rajvee -- O'Regan, Paul -- West, Stephen C -- New York, N.Y. -- Science. 2004 Jan 9;303(5655):243-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK, London Research Institute, Clare Hall Laboratories, South Mimms, Hertfordshire EN6 3LD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14716019" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; CHO Cells ; Cell Line ; Cricetinae ; DNA Repair ; DNA, Cruciform/chemistry/*metabolism ; DNA-Binding Proteins/chemistry/genetics/isolation & purification/*metabolism ; Electrophoresis, Polyacrylamide Gel ; Female ; HeLa Cells ; Holliday Junction Resolvases/*metabolism ; Humans ; Mutation ; Protein Structure, Tertiary ; Recombinant Proteins/metabolism ; Recombination, Genetic
    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
    Stress-dependent regulation of FOXO transcription factors by the SIRT1 deacetylase (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-21
    Description: The Sir2 deacetylase modulates organismal life-span in various species. However, the molecular mechanisms by which Sir2 increases longevity are largely unknown. We show that in mammalian cells, the Sir2 homolog SIRT1 appears to control the cellular response to stress by regulating the FOXO family of Forkhead transcription factors, a family of proteins that function as sensors of the insulin signaling pathway and as regulators of organismal longevity. SIRT1 and the FOXO transcription factor FOXO3 formed a complex in cells in response to oxidative stress, and SIRT1 deacetylated FOXO3 in vitro and within cells. SIRT1 had a dual effect on FOXO3 function: SIRT1 increased FOXO3's ability to induce cell cycle arrest and resistance to oxidative stress but inhibited FOXO3's ability to induce cell death. Thus, one way in which members of the Sir2 family of proteins may increase organismal longevity is by tipping FOXO-dependent responses away from apoptosis and toward stress resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunet, Anne -- Sweeney, Lora B -- Sturgill, J Fitzhugh -- Chua, Katrin F -- Greer, Paul L -- Lin, Yingxi -- Tran, Hien -- Ross, Sarah E -- Mostoslavsky, Raul -- Cohen, Haim Y -- Hu, Linda S -- Cheng, Hwei-Ling -- Jedrychowski, Mark P -- Gygi, Steven P -- Sinclair, David A -- Alt, Frederick W -- Greenberg, Michael E -- NIHP30-HD18655/HD/NICHD NIH HHS/ -- P01 NS35138-17/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Mar 26;303(5666):2011-5. Epub 2004 Feb 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Center for Blood Research (CBR) Institute for Biomedical Research, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14976264" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Apoptosis ; Cell Cycle ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Cerebellum/cytology ; Forkhead Transcription Factors ; Gene Expression Profiling ; Gene Expression Regulation ; Histone Deacetylases/genetics/*metabolism ; Humans ; Intracellular Signaling Peptides and Proteins ; Mice ; Mice, Knockout ; Neurons/cytology ; *Oxidative Stress ; Phosphorylation ; Proteins/genetics ; Recombinant Proteins/metabolism ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
    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
  • 6
    facet.materialart.
    Unknown
    Visfatin: a protein secreted by visceral fat that mimics the effects of insulin (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: Fat tissue produces a variety of secreted proteins (adipocytokines) with important roles in metabolism. We isolated a newly identified adipocytokine, visfatin, that is highly enriched in the visceral fat of both humans and mice and whose expression level in plasma increases during the development of obesity. Visfatin corresponds to a protein identified previously as pre-B cell colony-enhancing factor (PBEF), a 52-kilodalton cytokine expressed in lymphocytes. Visfatin exerted insulin-mimetic effects in cultured cells and lowered plasma glucose levels in mice. Mice heterozygous for a targeted mutation in the visfatin gene had modestly higher levels of plasma glucose relative to wild-type littermates. Surprisingly, visfatin binds to and activates the insulin receptor. Further study of visfatin's physiological role may lead to new insights into glucose homeostasis and/or new therapies for metabolic disorders such as diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukuhara, Atsunori -- Matsuda, Morihiro -- Nishizawa, Masako -- Segawa, Katsumori -- Tanaka, Masaki -- Kishimoto, Kae -- Matsuki, Yasushi -- Murakami, Mirei -- Ichisaka, Tomoko -- Murakami, Hiroko -- Watanabe, Eijiro -- Takagi, Toshiyuki -- Akiyoshi, Megumi -- Ohtsubo, Tsuguteru -- Kihara, Shinji -- Yamashita, Shizuya -- Makishima, Makoto -- Funahashi, Tohru -- Yamanaka, Shinya -- Hiramatsu, Ryuji -- Matsuzawa, Yuji -- Shimomura, Iichiro -- New York, N.Y. -- Science. 2005 Jan 21;307(5708):426-30. Epub 2004 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and Pathophysiology, Graduate School of Medicine, and Department of Organismal Biosystems, Graduate School of Frontier Biosciences, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604363" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/drug effects/metabolism ; Adipose Tissue/*metabolism ; Animals ; Binding Sites ; Blood Glucose/analysis ; Cell Line ; Cells, Cultured ; Cytokines/blood/genetics/*metabolism/pharmacology ; Diabetes Mellitus, Type 2/metabolism ; Dose-Response Relationship, Drug ; Female ; Gene Expression Profiling ; Gene Expression Regulation/drug effects ; Gene Targeting ; Humans ; Insulin/blood/*metabolism ; Insulin Resistance ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Molecular Mimicry ; Muscle Cells/metabolism ; Nicotinamide Phosphoribosyltransferase ; Phosphorylation ; Receptor, Insulin/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; Subcutaneous Tissue ; Viscera
    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
  • 7
    facet.materialart.
    Unknown
    Stem cell research in Korea (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Sang-yong -- New York, N.Y. -- Science. 2004 Aug 13;305(5686):944-5; author reply 944-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15310877" target="_blank"〉PubMed〈/a〉
    Keywords: Bioethical Issues ; Blastocyst/*cytology ; Cell Line ; Cloning, Organism/*ethics ; Embryo Research/*ethics ; Embryo, Mammalian/cytology ; Ethics Committees ; Ethics Committees, Research ; Humans ; Korea ; *Pluripotent Stem Cells
    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
  • 8
    facet.materialart.
    Unknown
    SUMO modification of Huntingtin and Huntington's disease pathology (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-06
    Description: Huntington's disease (HD) is characterized by the accumulation of a pathogenic protein, Huntingtin (Htt), that contains an abnormal polyglutamine expansion. Here, we report that a pathogenic fragment of Htt (Httex1p) can be modified either by small ubiquitin-like modifier (SUMO)-1 or by ubiquitin on identical lysine residues. In cultured cells, SUMOylation stabilizes Httex1p, reduces its ability to form aggregates, and promotes its capacity to repress transcription. In a Drosophila model of HD, SUMOylation of Httex1p exacerbates neurodegeneration, whereas ubiquitination of Httex1p abrogates neurodegeneration. Lysine mutations that prevent both SUMOylation and ubiquitination of Httex1p reduce HD pathology, indicating that the contribution of SUMOylation to HD pathology extends beyond preventing Htt ubiquitination and degradation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steffan, Joan S -- Agrawal, Namita -- Pallos, Judit -- Rockabrand, Erica -- Trotman, Lloyd C -- Slepko, Natalia -- Illes, Katalin -- Lukacsovich, Tamas -- Zhu, Ya-Zhen -- Cattaneo, Elena -- Pandolfi, Pier Paolo -- Thompson, Leslie Michels -- Marsh, J Lawrence -- CA-62203/CA/NCI NIH HHS/ -- HD36049/HD/NICHD NIH HHS/ -- HD36081/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2004 Apr 2;304(5667):100-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Human Behavior, Gillespie 2121, University of California, Irvine, CA 92697, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15064418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Cell Line ; Cell Nucleus/metabolism ; Corpus Striatum/cytology ; Cytoplasm/metabolism ; Drosophila ; Genes, MDR ; HeLa Cells ; Humans ; Huntington Disease/metabolism/*pathology ; Lysine/genetics/metabolism ; Mutation ; Nerve Degeneration ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neurons/metabolism ; Nuclear Proteins/chemistry/genetics/*metabolism ; Proline/genetics/metabolism ; Promoter Regions, Genetic ; Rats ; Recombinant Fusion Proteins/metabolism ; SUMO-1 Protein/genetics/*metabolism ; Transcription, Genetic ; Transfection ; Ubiquitin/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
  • 9
    facet.materialart.
    Unknown
    T cell activation by lipopeptide antigens (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-24
    Description: Unlike major histocompatibility proteins, which bind peptides, CD1 proteins display lipid antigens to T cells. Here, we report that CD1a presents a family of previously unknown lipopeptides from Mycobacterium tuberculosis, named didehydroxymycobactins because of their structural relation to mycobactin siderophores. T cell activation was mediated by the alphabeta T cell receptors and was specific for structure of the acyl and peptidic components of these antigens. These studies identify a means of intracellular pathogen detection and identify lipopeptides as a biochemical class of antigens for T cells, which, like conventional peptides, have a potential for marked structural diversity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moody, D Branch -- Young, David C -- Cheng, Tan-Yun -- Rosat, Jean-Pierre -- Roura-Mir, Carme -- O'Connor, Peter B -- Zajonc, Dirk M -- Walz, Andrew -- Miller, Marvin J -- Levery, Steven B -- Wilson, Ian A -- Costello, Catherine E -- Brenner, Michael B -- AI30988/AI/NIAID NIH HHS/ -- AI50216/AI/NIAID NIH HHS/ -- AR48632/AR/NIAMS NIH HHS/ -- CA58896/CA/NCI NIH HHS/ -- GM25845/GM/NIGMS NIH HHS/ -- GM62116/GM/NIGMS NIH HHS/ -- P20 RR16459/RR/NCRR NIH HHS/ -- P41-RR10888/RR/NCRR NIH HHS/ -- S10-RR10493/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2004 Jan 23;303(5657):527-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital and Harvard Medical School, Smith Building Room 514, 1 Jimmy Fund Way, Boston, MA 02115, USA. bmoody@rics.bwh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14739458" target="_blank"〉PubMed〈/a〉
    Keywords: *Antigen Presentation ; Antigens, Bacterial/chemistry/*immunology/metabolism ; Antigens, CD1/chemistry/immunology/metabolism ; Cell Line ; Chromatography, High Pressure Liquid ; Humans ; Hydrogen Bonding ; Hydrophobic and Hydrophilic Interactions ; Hydroxylation ; Lipoproteins/chemistry/*immunology/metabolism ; *Lymphocyte Activation ; Models, Molecular ; Mycobacterium tuberculosis/growth & development/*immunology ; Oxazoles/chemistry/*immunology/metabolism ; Protein Conformation ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/*immunology ; Transfection
    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
  • 10
    facet.materialart.
    Unknown
    Endothelial cells stimulate self-renewal and expand neurogenesis of neural stem cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-03
    Description: Neural stem cells are reported to lie in a vascular niche, but there is no direct evidence for a functional relationship between the stem cells and blood vessel component cells. We show that endothelial cells but not vascular smooth muscle cells release soluble factors that stimulate the self-renewal of neural stem cells, inhibit their differentiation, and enhance their neuron production. Both embryonic and adult neural stem cells respond, allowing extensive production of both projection neuron and interneuron types in vitro. Endothelial coculture stimulates neuroepithelial cell contact, activating Notch and Hes 1 to promote self-renewal. These findings identify endothelial cells as a critical component of the neural stem cell niche.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Qin -- Goderie, Susan K -- Jin, Li -- Karanth, Nithin -- Sun, Yu -- Abramova, Natalia -- Vincent, Peter -- Pumiglia, Kevin -- Temple, Sally -- R01 CA081419/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2004 May 28;304(5675):1338-40. Epub 2004 Apr 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, NY 12208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15060285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology/physiology ; Cattle ; Cell Adhesion ; *Cell Communication ; Cell Differentiation ; Cell Division ; Cell Line ; Cell Lineage ; Cells, Cultured ; Cerebral Cortex/embryology ; Clone Cells/physiology ; Coculture Techniques ; Embryo, Mammalian/cytology ; Endothelial Cells/cytology/*physiology ; Endothelium, Vascular/cytology ; Fibroblast Growth Factor 2/pharmacology ; Mice ; Muscle, Smooth, Vascular/cytology/physiology ; Myocytes, Smooth Muscle/cytology/physiology ; Neurons/cytology/*physiology ; Oligodendroglia/cytology/physiology ; Signal Transduction ; Stem Cells/cytology/*physiology
    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
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...