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  • Articles  (165)
  • Mice  (165)
  • 2005-2009  (165)
  • 2008  (165)
  • Physics  (165)
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  • Articles  (165)
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  • 2005-2009  (165)
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  • 1
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    Label-free biomedical imaging with high sensitivity by stimulated Raman scattering microscopy (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-20
    Description: 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〉
    Keywords: 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
    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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    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
    Publication Date: 2008-12-20
    Description: 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〉
    Keywords: 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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Germ cell-intrinsic and -extrinsic factors govern meiotic initiation in mouse embryos (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-17
    Description: 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〉
    Keywords: 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
    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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    Structure and functional role of dynein's microtubule-binding domain (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-17
    Description: 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〉
    Keywords: 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
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  • 5
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    A mouse speciation gene encodes a meiotic histone H3 methyltransferase (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-17
    Description: 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〉
    Keywords: 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
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  • 6
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    The sphingolipid transporter spns2 functions in migration of zebrafish myocardial precursors (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-17
    Description: 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〉
    Keywords: 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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Immunology. Chaperone puts the brakes on (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-17
    Description: 〈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〉
    Keywords: 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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Regulation of dendritic cell migration by CD74, the MHC class II-associated invariant chain (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-17
    Description: Dendritic cells (DCs) sample peripheral tissues of the body in search of antigens to present to T cells. This requires two processes, antigen processing and cell motility, originally thought to occur independently. We found that the major histocompatibility complex II-associated invariant chain (Ii or CD74), a known regulator of antigen processing, negatively regulates DC motility in vivo. By using microfabricated channels to mimic the confined environment of peripheral tissues, we found that wild-type DCs alternate between high and low motility, whereas Ii-deficient cells moved in a faster and more uniform manner. The regulation of cell motility by Ii depended on the actin-based motor protein myosin II. Coupling antigen processing and cell motility may enable DCs to more efficiently detect and process antigens within a defined space.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faure-Andre, Gabrielle -- Vargas, Pablo -- Yuseff, Maria-Isabel -- Heuze, Melina -- Diaz, Jheimmy -- Lankar, Danielle -- Steri, Veronica -- Manry, Jeremy -- Hugues, Stephanie -- Vascotto, Fulvia -- Boulanger, Jerome -- Raposo, Graca -- Bono, Maria-Rosa -- Rosemblatt, Mario -- Piel, Matthieu -- Lennon-Dumenil, Ana-Maria -- New York, N.Y. -- Science. 2008 Dec 12;322(5908):1705-10. doi: 10.1126/science.1159894.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U653, Institut Curie, 12 rue Lhomond, 75005, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19074353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens, Differentiation, B-Lymphocyte/genetics/*metabolism ; Cathepsins/genetics/metabolism ; *Cell Movement ; Dendritic Cells/*immunology/physiology ; Endocytosis ; Histocompatibility Antigens Class II/genetics/*metabolism ; Lipopolysaccharides/immunology ; Lymph Nodes/cytology/immunology ; Lysosomes/metabolism ; Mice ; Mice, Inbred C57BL ; Myosin Type II/*metabolism ; Phosphorylation
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  • 9
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    A stress signaling pathway in adipose tissue regulates hepatic insulin resistance (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: A high-fat diet causes activation of the regulatory protein c-Jun NH2-terminal kinase 1 (JNK1) and triggers development of insulin resistance. JNK1 is therefore a potential target for therapeutic treatment of metabolic syndrome. We explored the mechanism of JNK1 signaling by engineering mice in which the Jnk1 gene was ablated selectively in adipose tissue. JNK1 deficiency in adipose tissue suppressed high-fat diet-induced insulin resistance in the liver. JNK1-dependent secretion of the inflammatory cytokine interleukin-6 by adipose tissue caused increased expression of liver SOCS3, a protein that induces hepatic insulin resistance. Thus, JNK1 activation in adipose tissue can cause insulin resistance in the liver.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643026/" 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/PMC2643026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabio, Guadalupe -- Das, Madhumita -- Mora, Alfonso -- Zhang, Zhiyou -- Jun, John Y -- Ko, Hwi Jin -- Barrett, Tamera -- Kim, Jason K -- Davis, Roger J -- DK52530/DK/NIDDK NIH HHS/ -- R01 CA065861/CA/NCI NIH HHS/ -- R01 CA065861-14/CA/NCI NIH HHS/ -- R01 DK080756/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1539-43. doi: 10.1126/science.1160794.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056984" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/enzymology/*metabolism ; Adipose Tissue/enzymology/metabolism ; Animals ; Dietary Fats/administration & dosage ; Enzyme Activation ; Glucose/metabolism ; Insulin/metabolism ; Insulin Receptor Substrate Proteins/metabolism ; *Insulin Resistance ; Interleukin-6/administration & dosage/metabolism ; Liver/*metabolism ; MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 8/deficiency/genetics/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; *Signal Transduction ; *Stress, Physiological ; Suppressor of Cytokine Signaling Proteins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Activation of pannexin-1 hemichannels augments aberrant bursting in the hippocampus (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: Pannexin-1 (Px1) is expressed at postsynaptic sites in pyramidal neurons, suggesting that these hemichannels contribute to dendritic signals associated with synaptic function. We found that, in pyramidal neurons, N-methyl-d-aspartate receptor (NMDAR) activation induced a secondary prolonged current and dye flux that were blocked with a specific inhibitory peptide against Px1 hemichannels; knockdown of Px1 by RNA interference blocked the current in cultured neurons. Enhancing endogenous NMDAR activation in brain slices by removing external magnesium ions (Mg2+) triggered epileptiform activity, which had decreased spike amplitude and prolonged interburst interval during application of the Px1 hemichannel blocking peptide. We conclude that Px1 hemichannel opening is triggered by NMDAR stimulation and can contribute to epileptiform seizure activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Roger J -- Jackson, Michael F -- Olah, Michelle E -- Rungta, Ravi L -- Hines, Dustin J -- Beazely, Michael A -- MacDonald, John F -- MacVicar, Brian A -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1555-9. doi: 10.1126/science.1165209.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Brain Research Centre, University of British Columbia, 2211 Wesbrook Mall, Vancouver, BC V6T 2B5, Canada. rj.thompson@ucalgary.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056988" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Adenosine Triphosphate/metabolism ; Animals ; Calcium/metabolism ; Cells, Cultured ; Connexins/genetics/*physiology ; Dendrites/physiology ; Electrical Synapses/physiology ; Epilepsy/physiopathology ; Hippocampus/*physiology/physiopathology ; In Vitro Techniques ; Mice ; Nerve Tissue Proteins/genetics/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; RNA Interference ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Synaptic Transmission
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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