ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
Filter
  • Artikel  (236)
  • Mice  (165)
  • Molecular Sequence Data  (88)
  • 2005-2009  (236)
  • 2008  (236)
  • Physik  (236)
Sammlung
  • Artikel  (236)
Datenquelle
Schlagwörter
Verlag/Herausgeber
Erscheinungszeitraum
  • 2005-2009  (236)
Jahr
Zeitschrift
Thema
  • 1
    facet.materialart.
    Unbekannt
    Label-free biomedical imaging with high sensitivity by stimulated Raman scattering microscopy (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-12-20
    Beschreibung: Label-free chemical contrast is highly desirable in biomedical imaging. Spontaneous Raman microscopy provides specific vibrational signatures of chemical bonds, but is often hindered by low sensitivity. Here we report a three-dimensional multiphoton vibrational imaging technique based on stimulated Raman scattering (SRS). The sensitivity of SRS imaging is significantly greater than that of spontaneous Raman microscopy, which is achieved by implementing high-frequency (megahertz) phase-sensitive detection. SRS microscopy has a major advantage over previous coherent Raman techniques in that it offers background-free and readily interpretable chemical contrast. We show a variety of biomedical applications, such as differentiating distributions of omega-3 fatty acids and saturated lipids in living cells, imaging of brain and skin tissues based on intrinsic lipid contrast, and monitoring drug delivery through the epidermis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576036/" 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/PMC3576036/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freudiger, Christian W -- Min, Wei -- Saar, Brian G -- Lu, Sijia -- Holtom, Gary R -- He, Chengwei -- Tsai, Jason C -- Kang, Jing X -- Xie, X Sunney -- CA113605/CA/NCI NIH HHS/ -- DP1 OD000277/OD/NIH HHS/ -- DP1 OD000277-05/OD/NIH HHS/ -- R01 CA113605/CA/NCI NIH HHS/ -- R01 CA113605-01A2/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1857-61. doi: 10.1126/science.1165758.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19095943" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line, Tumor ; Corpus Callosum/chemistry/cytology ; Dimethyl Sulfoxide/administration & dosage/pharmacokinetics ; Eicosapentaenoic Acid/metabolism ; Epidermis/chemistry/metabolism/ultrastructure ; Humans ; Imaging, Three-Dimensional/*methods ; Lipids/*analysis ; Mice ; Microscopy/*methods ; Neurons/ultrastructure ; Sensitivity and Specificity ; Skin/chemistry/ultrastructure ; *Spectrum Analysis, Raman ; Tretinoin/administration & dosage/pharmacokinetics ; Vitamin A/analysis/chemistry
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 2
    facet.materialart.
    Unbekannt
    Leukemic cells create bone marrow niches that disrupt the behavior of normal hematopoietic progenitor cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-12-20
    Beschreibung: The host tissue microenvironment influences malignant cell proliferation and metastasis, but little is known about how tumor-induced changes in the microenvironment affect benign cellular ecosystems. Applying dynamic in vivo imaging to a mouse model, we show that leukemic cell growth disrupts normal hematopoietic progenitor cell (HPC) bone marrow niches and creates abnormal microenvironments that sequester transplanted human CD34+ (HPC-enriched) cells. CD34+ cells in leukemic mice declined in number over time and failed to mobilize into the peripheral circulation in response to cytokine stimulation. Neutralization of stem cell factor (SCF) secreted by leukemic cells inhibited CD34+ cell migration into malignant niches, normalized CD34+ cell numbers, and restored CD34+ cell mobilization in leukemic mice. These data suggest that the tumor microenvironment causes HPC dysfunction by usurping normal HPC niches and that therapeutic inhibition of HPC interaction with tumor niches may help maintain normal progenitor cell function in the setting of malignancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colmone, Angela -- Amorim, Maria -- Pontier, Andrea L -- Wang, Sheng -- Jablonski, Elizabeth -- Sipkins, Dorothy A -- 1DP2OD002160-01/OD/NIH HHS/ -- 5K08CA112126-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1861-5. doi: 10.1126/science.1164390.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Section of Hematology/Oncology, University of Chicago, 5841 South Maryland Avenue MC 2115, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19095944" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, CD34/analysis ; Bone Marrow/*pathology ; Cell Count ; Cell Line, Tumor ; Cell Movement ; Chemokine CXCL12/metabolism ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/metabolism/*physiology ; Heterocyclic Compounds/pharmacology ; Humans ; Leukemia, Myeloid, Acute/metabolism/*pathology ; Mice ; Mice, SCID ; Neoplasm Transplantation ; Precursor B-Cell Lymphoblastic ; Leukemia-Lymphoma/metabolism/*pathology/physiopathology ; Stem Cell Factor/genetics/metabolism ; Stem Cell Niche/*pathology/physiopathology ; Transplantation, Heterologous ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 3
    facet.materialart.
    Unbekannt
    A conserved molecular framework for compound leaf development (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-12-20
    Beschreibung: Diversity in leaf shape is produced by alterations of the margin: for example, deep dissection leads to leaflet formation and less-pronounced incision results in serrations or lobes. By combining gene silencing and mutant analyses in four distantly related eudicot species, we show that reducing the function of NAM/CUC boundary genes (NO APICAL MERISTEM and CUP-SHAPED COTYLEDON) leads to a suppression of all marginal outgrowths and to fewer and fused leaflets. We propose that NAM/CUC genes promote formation of a boundary domain that delimits leaflets. This domain has a dual role promoting leaflet separation locally and leaflet formation at distance. In this manner, boundaries of compound leaves resemble boundaries functioning during animal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blein, Thomas -- Pulido, Amada -- Vialette-Guiraud, Aurelie -- Nikovics, Krisztina -- Morin, Halima -- Hay, Angela -- Johansen, Ida Elisabeth -- Tsiantis, Miltos -- Laufs, Patrick -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1835-9. doi: 10.1126/science.1166168.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Biologie Cellulaire, Institut Jean Pierre Bourgin, Institut National de la Recherche Agronomique (INRA), 78026 Versailles Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19095941" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Aquilegia/genetics/growth & development/metabolism ; Cardamine/genetics/growth & development/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Plant ; Gene Silencing ; *Genes, Plant ; Lycopersicon esculentum/genetics/growth & development/metabolism ; Molecular Sequence Data ; Peas/genetics/growth & development ; Phylogeny ; Plant Leaves/genetics/*growth & development/metabolism ; Plant Proteins/genetics/metabolism ; Plants, Genetically Modified ; Solanum tuberosum/genetics/growth & development/metabolism ; Transcription Factors/chemistry/*genetics/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 4
    facet.materialart.
    Unbekannt
    Rapid membrane disruption by a perforin-like protein facilitates parasite exit from host cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-12-20
    Beschreibung: Perforin-like proteins are expressed by many bacterial and protozoan pathogens, yet little is known about their function or mode of action. Here, we describe Toxoplasma perforin-like protein 1 (TgPLP1), a secreted perforin-like protein of the intracellular protozoan pathogen Toxoplasma gondii that displays structural features necessary for pore formation. After intracellular growth, TgPLP1-deficient parasites failed to exit normally, resulting in entrapment within host cells. We show that this defect is due to an inability to rapidly permeabilize the parasitophorous vacuole membrane and host plasma membrane during exit. TgPLP1 ablation had little effect on growth in culture but resulted in a reduction greater than five orders of magnitude of acute virulence in mice. Perforin-like proteins from other intracellular pathogens may play a similar role in microbial egress and virulence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2662845/" 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/PMC2662845/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kafsack, Bjorn F C -- Pena, Janethe D O -- Coppens, Isabelle -- Ravindran, Sandeep -- Boothroyd, John C -- Carruthers, Vern B -- R01 AI021423/AI/NIAID NIH HHS/ -- R01 AI046675/AI/NIAID NIH HHS/ -- R01 AI046675-06/AI/NIAID NIH HHS/ -- R01 AI046675-07/AI/NIAID NIH HHS/ -- R01 AI046675-08/AI/NIAID NIH HHS/ -- R01 AI046675-09/AI/NIAID NIH HHS/ -- R01 AI46675/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 23;323(5913):530-3. doi: 10.1126/science.1165740. Epub 2008 Dec 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19095897" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Calcimycin/pharmacology ; Cell Membrane/*metabolism ; Cell Membrane Permeability ; Cells, Cultured ; Host-Parasite Interactions ; Humans ; Intracellular Membranes/*metabolism ; Ionophores/pharmacology ; Models, Molecular ; Molecular Sequence Data ; Perforin/chemistry/genetics/*metabolism ; Permeability ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protozoan Proteins/chemistry/genetics/*metabolism ; Toxoplasma/genetics/growth & development/*metabolism/pathogenicity ; Vacuoles/*metabolism/*parasitology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 5
    facet.materialart.
    Unbekannt
    Germ cell-intrinsic and -extrinsic factors govern meiotic initiation in mouse embryos (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-12-17
    Beschreibung: Retinoic acid (RA) is an essential extrinsic inducer of meiotic initiation in mammalian germ cells. However, RA acts too widely in mammalian development to account, by itself, for the cell-type and temporal specificity of meiotic initiation. We considered parallels to yeast, in which extrinsic and intrinsic factors combine to restrict meiotic initiation. We demonstrate that, in mouse embryos, extrinsic and intrinsic factors together regulate meiotic initiation. The mouse RNA-binding protein DAZL, which is expressed by postmigratory germ cells, is a key intrinsic factor, enabling those cells to initiate meiosis in response to RA. Within a brief developmental window, Dazl-expressing germ cells in both XX and XY embryos actively acquire the ability to interpret RA as a meiosis-inducing signal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Yanfeng -- Gill, Mark E -- Koubova, Jana -- Page, David C -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Dec 12;322(5908):1685-7. doi: 10.1126/science.1166340.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Whitehead Institute, and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19074348" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptor Proteins, Signal Transducing ; Animals ; Cell Cycle Proteins/metabolism ; Cell Nucleus/ultrastructure ; DNA Breaks ; DNA Repair ; Embryo, Mammalian/*cytology/physiology ; Endodeoxyribonucleases ; Esterases/metabolism ; Female ; Germ Cells/*cytology ; Male ; *Meiosis ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/genetics/metabolism ; Ovary/embryology/physiology ; Phosphoproteins/genetics/metabolism ; Proteins/metabolism ; RNA-Binding Proteins/genetics/*physiology ; Testis/embryology/physiology ; Tretinoin/pharmacology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 6
    facet.materialart.
    Unbekannt
    Structure and functional role of dynein's microtubule-binding domain (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-12-17
    Beschreibung: Dynein motors move various cargos along microtubules within the cytoplasm and power the beating of cilia and flagella. An unusual feature of dynein is that its microtubule-binding domain (MTBD) is separated from its ring-shaped AAA+ adenosine triphosphatase (ATPase) domain by a 15-nanometer coiled-coil stalk. We report the crystal structure of the mouse cytoplasmic dynein MTBD and a portion of the coiled coil, which supports a mechanism by which the ATPase domain and MTBD may communicate through a shift in the heptad registry of the coiled coil. Surprisingly, functional data suggest that the MTBD, and not the ATPase domain, is the main determinant of the direction of dynein motility.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2663340/" 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/PMC2663340/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carter, Andrew P -- Garbarino, Joan E -- Wilson-Kubalek, Elizabeth M -- Shipley, Wesley E -- Cho, Carol -- Milligan, Ronald A -- Vale, Ronald D -- Gibbons, I R -- GM30401-29/GM/NIGMS NIH HHS/ -- GM52468/GM/NIGMS NIH HHS/ -- P01 AR042895/AR/NIAMS NIH HHS/ -- P01 AR042895-15/AR/NIAMS NIH HHS/ -- P01-AR42895/AR/NIAMS NIH HHS/ -- P41 RR-17573/RR/NCRR NIH HHS/ -- R01 GM097312/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Dec 12;322(5908):1691-5. doi: 10.1126/science.1164424.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19074350" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Animals ; Binding Sites ; Crystallization ; Crystallography, X-Ray ; Dimerization ; Dyneins/*chemistry/*metabolism ; Hydrophobic and Hydrophilic Interactions ; Image Processing, Computer-Assisted ; Mice ; Microscopy, Electron ; Microtubules/*metabolism/ultrastructure ; Models, Molecular ; Molecular Sequence Data ; Movement ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/chemistry/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 7
    facet.materialart.
    Unbekannt
    A single gene causes both male sterility and segregation distortion in Drosophila hybrids (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-12-17
    Beschreibung: A central goal of evolutionary biology is to identify the genes and evolutionary forces that cause speciation, the emergence of reproductive isolation between populations. Despite the identification of several genes that cause hybrid sterility or inviability-many of which have evolved rapidly under positive Darwinian selection-little is known about the ecological or genomic forces that drive the evolution of postzygotic isolation. Here, we show that the same gene, Overdrive, causes both male sterility and segregation distortion in F1 hybrids between the Bogota and U.S. subspecies of Drosophila pseudoobscura. This segregation distorter gene is essential for hybrid sterility, a strong reproductive barrier between these young taxa. Our results suggest that genetic conflict may be an important evolutionary force in speciation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628965/" 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/PMC2628965/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Phadnis, Nitin -- Orr, H Allen -- GM51932/GM/NIGMS NIH HHS/ -- R01 GM051932/GM/NIGMS NIH HHS/ -- R01 GM051932-13/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 16;323(5912):376-9. doi: 10.1126/science.1163934. Epub 2008 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Rochester, Rochester, NY 14627-0211, USA. pdns@mail.rochester.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19074311" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Carrier Proteins/chemistry/*genetics/physiology ; Chromosome Mapping ; Chromosome Segregation/*genetics ; Crosses, Genetic ; Drosophila/*genetics ; Drosophila Proteins/chemistry/*genetics/physiology ; Female ; Gene Flow ; *Genes, Insect ; *Genetic Speciation ; *Hybridization, Genetic ; Infertility, Male/genetics ; Male ; Meiosis ; Microsatellite Repeats ; Molecular Sequence Data ; Sex Ratio ; Transgenes
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 8
    facet.materialart.
    Unbekannt
    A mouse speciation gene encodes a meiotic histone H3 methyltransferase (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-12-17
    Beschreibung: Speciation genes restrict gene flow between the incipient species and related taxa. Three decades ago, we mapped a mammalian speciation gene, hybrid sterility 1 (Hst1), in the intersubspecific hybrids of house mouse. Here, we identify this gene as Prdm9, encoding a histone H3 lysine 4 trimethyltransferase. We rescued infertility in male hybrids with bacterial artificial chromosomes carrying Prdm9 from a strain with the "fertility" Hst1(f) allele. Sterile hybrids display down-regulated microrchidia 2B (Morc2b) and fail to compartmentalize gammaH2AX into the pachynema sex (XY) body. These defects, seen also in Prdm9-null mutants, are rescued by the Prdm9 transgene. Identification of a vertebrate hybrid sterility gene reveals a role for epigenetics in speciation and opens a window to a hybrid sterility gene network.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mihola, Ondrej -- Trachtulec, Zdenek -- Vlcek, Cestmir -- Schimenti, John C -- Forejt, Jiri -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Jan 16;323(5912):373-5. doi: 10.1126/science.1163601. Epub 2008 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague, Czech Republic.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19074312" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Chromosome Mapping ; Chromosomes, Artificial, Bacterial ; Crosses, Genetic ; Epigenesis, Genetic ; Female ; Gene Expression Regulation ; *Genetic Speciation ; Histone-Lysine N-Methyltransferase/chemistry/*genetics/*metabolism ; Histones/metabolism ; Hybridization, Genetic ; Infertility, Male/*genetics ; Male ; *Meiosis ; Methylation ; Mice ; Mice, Inbred C3H ; Mice, Transgenic ; Molecular Sequence Data ; Ovary/enzymology ; Testis/enzymology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 9
    facet.materialart.
    Unbekannt
    The sphingolipid transporter spns2 functions in migration of zebrafish myocardial precursors (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-12-17
    Beschreibung: Sphingosine-1-phosphate (S1P) is a secreted lipid mediator that functions in vascular development; however, it remains unclear how S1P secretion is regulated during embryogenesis. We identified a zebrafish mutant, ko157, that displays cardia bifida (two hearts) resembling that in the S1P receptor-2 mutant. A migration defect of myocardial precursors in the ko157 mutant is due to a mutation in a multipass transmembrane protein, Spns2, and can be rescued by S1P injection. We show that the export of S1P from cells requires Spns2. spns2 is expressed in the extraembryonic tissue yolk syncytial layer (YSL), and the introduction of spns2 mRNA in the YSL restored the cardiac defect in the ko157 mutant. Thus, Spns2 in the YSL functions as a S1P transporter in S1P secretion, thereby regulating myocardial precursor migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawahara, Atsuo -- Nishi, Tsuyoshi -- Hisano, Yu -- Fukui, Hajime -- Yamaguchi, Akihito -- Mochizuki, Naoki -- New York, N.Y. -- Science. 2009 Jan 23;323(5913):524-7. doi: 10.1126/science.1167449. Epub 2008 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Structural Analysis, National Cardiovascular Center Research Institute, Fujishirodai 5-7-1, Suita, Osaka 565-8565, Japan. atsuo@ri.ncvc.go.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19074308" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Animals, Genetically Modified ; Blastomeres/metabolism ; CHO Cells ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Movement ; Cricetinae ; Cricetulus ; Embryo, Nonmammalian/cytology/*metabolism ; Embryonic Development ; Heart/*embryology ; Heart Defects, Congenital/embryology ; Humans ; Lysophospholipids/*metabolism ; Membrane Proteins/chemistry/genetics/*metabolism ; Mesoderm/metabolism ; Mice ; Molecular Sequence Data ; Mutation ; Oligonucleotides, Antisense ; Organogenesis ; Signal Transduction ; Somites/embryology/metabolism ; Sphingosine/*analogs & derivatives/metabolism ; Zebrafish/*embryology/genetics ; Zebrafish Proteins/chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 10
    facet.materialart.
    Unbekannt
    Immunology. Chaperone puts the brakes on (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-12-17
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lukacs-Kornek, Veronika -- Turley, Shannon J -- New York, N.Y. -- Science. 2008 Dec 12;322(5908):1640-1. doi: 10.1126/science.1168103.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Immunology and AIDS, Dana Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19074333" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigen Presentation ; Antigens, Differentiation, B-Lymphocyte/chemistry/*metabolism ; Cathepsins/metabolism ; Cell Membrane/immunology/metabolism ; *Cell Movement ; Dendritic Cells/*immunology/physiology ; Histocompatibility Antigens Class II/chemistry/immunology/*metabolism ; *Lymphocyte Activation ; Lysosomes/metabolism ; Mice ; Molecular Motor Proteins/metabolism ; Myosin Type II/metabolism ; T-Lymphocytes/*immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...