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  • 1
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    Lysophosphatidylcholine as a ligand for the immunoregulatory receptor G2A (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-07-28
    Description: Although the biological actions of the cell membrane and serum lipid lysophosphatidylcholine (LPC) in atherosclerosis and systemic autoimmune disease are well recognized, LPC has not been linked to a specific cell-surface receptor. We show that LPC is a high-affinity ligand for G2A, a lymphocyte-expressed G protein-coupled receptor whose genetic ablation results in the development of autoimmunity. Activation of G2A by LPC increased intracellular calcium concentration, induced receptor internalization, activated ERK mitogen-activated protein kinase, and modified migratory responses of Jurkat T lymphocytes. This finding implicates a role for LPC-G2A interaction in the etiology of inflammatory autoimmune disease and atherosclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kabarowski, J H -- Zhu, K -- Le, L Q -- Witte, O N -- Xu, Y -- 1 R21 CA84038-01/CA/NCI NIH HHS/ -- CA76204/CA/NCI NIH HHS/ -- T32 CA09056/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2001 Jul 27;293(5530):702-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Immunology, and Molecular Genetics, Lerner Research Institute, 9500 Euclid Avenue, Cleveland, OH 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11474113" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arteriosclerosis/immunology/metabolism ; Calcium/metabolism ; Cell Cycle Proteins/*metabolism ; Cell Line ; Chemotaxis, Leukocyte ; Humans ; Jurkat Cells ; Ligands ; Lupus Erythematosus, Systemic/immunology/metabolism ; Lymphocyte Activation ; Lysophosphatidylcholines/*metabolism/pharmacology ; Mitogen-Activated Protein Kinases/metabolism ; Phosphorylcholine/analogs & derivatives/metabolism/pharmacology ; Radioligand Assay ; Receptors, Cell Surface/*metabolism ; *Receptors, G-Protein-Coupled ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Sphingosine/analogs & derivatives/metabolism/pharmacology ; T-Lymphocytes/immunology/*metabolism/physiology ; Tetradecanoylphorbol Acetate/pharmacology ; Transfection ; Virulence Factors, Bordetella/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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  • 2
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    A GDP dissociation inhibitor that serves as a GTPase inhibitor for the Ras-like protein CDC42Hs (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-30
    Description: Members of the family of Ras-related guanosine triphosphate (GTP) binding proteins appear to take part in the regulation of a number of biological processes, including cell growth and differentiation. Three different classes of proteins that regulate the GTP binding and GTP hydrolytic activities of the Ras family members have been identified. These different regulatory proteins inhibit guanosine diphosphate (GDP) dissociation (designated as GDIs), stimulate GDP dissociation and GDP-GTP exchange (designated as GDSs), or stimulate GTP hydrolysis (designated as GAPs). In the case of the Ras-like protein CDC42Hs, which is the human homolog of a Saccharomyces cerevisiae cell division cycle protein, the GDI protein also inhibited both the intrinsic and GAP-stimulated hydrolysis of GTP. These findings establish an additional role for the GDI protein--namely, as a guanosine triphosphatase (GTPase) inhibitory protein for a Ras-like GTP binding protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hart, M J -- Maru, Y -- Leonard, D -- Witte, O N -- Evans, T -- Cerione, R A -- New York, N.Y. -- Science. 1992 Oct 30;258(5083):812-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Cell, and Molecular Biology, Cornell University, Ithaca, NY 14853.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439791" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Platelets/chemistry ; Brain Chemistry ; Cattle ; Escherichia coli/genetics ; GTP Phosphohydrolases/*antagonists & inhibitors ; GTP-Binding Proteins/*antagonists & inhibitors/genetics/metabolism/*physiology ; GTPase-Activating Proteins ; *Guanine Nucleotide Dissociation Inhibitors ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Hydrolysis ; Membrane Proteins/metabolism ; Oncogene Proteins/metabolism ; *Protein-Tyrosine Kinases ; Proteins/metabolism ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcr ; Recombinant Fusion Proteins/metabolism ; cdc42 GTP-Binding Protein ; ras GTPase-Activating Proteins ; rho-Specific Guanine Nucleotide Dissociation Inhibitors ; rhoB GTP-Binding 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
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    Tyrosine kinase activity and transformation potency of bcr-abl oncogene products (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-02
    Description: Oncogenic activation of the proto-oncogene c-abl in human leukemias occurs as a result of the addition of exons from the gene bcr and truncation of the first abl exon. Analysis of tyrosine kinase activity and quantitative measurement of transformation potency in a single-step assay indicate that variation in bcr exon contribution results in a functional difference between p210bcr-abl and p185bcr-abl proteins. Thus, foreign upstream sequences are important in the deregulation of the kinase activity of the abl product, and the extent of deregulation correlates with the pathological effects of the bcr-abl proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lugo, T G -- Pendergast, A M -- Muller, A J -- Witte, O N -- 5T32GM07185/GM/NIGMS NIH HHS/ -- IT32GM08243/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 2;247(4946):1079-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2408149" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Southern ; Cell Line ; *Cell Transformation, Neoplastic/genetics ; Exons ; *Gene Expression Regulation, Neoplastic ; Leukemia, Experimental/genetics ; Protein-Tyrosine Kinases/genetics/*metabolism ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins c-abl ; Proto-Oncogene Proteins c-bcr ; Retroviridae/genetics
    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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    Initiation of deregulated growth of multipotent progenitor cells by bcr-abl in vitro (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-08
    Description: Expression of the bcr-abl oncogene in multipotent progenitor cells (MPPCs) is implicated as a key event in the development of chronic myelogenous leukemia. Bone marrow enriched for MPPCs was infected with a retrovirus that carried bcr-abl. The mixed-lineage colonies that resulted were responsive to growth factors and could differentiate. These cells later became growth factor-independent but, when injected into severe combined immunodeficient mice, were not leukemogenic. Thus, the presence of bcr-abl alone does not cause growth factor independence, although it initiates a stepwise process. This system may prove useful in the study of other oncogenes that cause leukemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gishizky, M L -- Witte, O N -- New York, N.Y. -- Science. 1992 May 8;256(5058):836-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1375394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/drug effects ; Bone Marrow Cells ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Clone Cells ; Drug Resistance, Microbial/genetics ; Fluorouracil/pharmacology ; Fusion Proteins, bcr-abl/*genetics ; Hematopoietic Cell Growth Factors/pharmacology ; Hematopoietic Stem Cells/*cytology/drug effects/physiology ; Humans ; Interleukin-3/pharmacology ; Macrophages/cytology/drug effects ; Mast Cells/cytology/drug effects ; Mice ; Rats ; Retroviridae/genetics ; Stem Cell Factor ; Transfection
    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
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    Identification of a cell of origin for human prostate cancer (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-31
    Description: Luminal cells are believed to be the cells of origin for human prostate cancer, because the disease is characterized by luminal cell expansion and the absence of basal cells. Yet functional studies addressing the origin of human prostate cancer have not previously been reported because of a lack of relevant in vivo human models. Here we show that basal cells from primary benign human prostate tissue can initiate prostate cancer in immunodeficient mice. The cooperative effects of AKT, ERG, and androgen receptor in basal cells recapitulated the histological and molecular features of human prostate cancer, with loss of basal cells and expansion of luminal cells expressing prostate-specific antigen and alpha-methylacyl-CoA racemase. Our results demonstrate that histological characterization of cancers does not necessarily correlate with the cellular origins of the disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917982/" 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/PMC2917982/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldstein, Andrew S -- Huang, Jiaoti -- Guo, Changyong -- Garraway, Isla P -- Witte, Owen N -- GM07185/GM/NIGMS NIH HHS/ -- P50 CA092131/CA/NCI NIH HHS/ -- P50 CA092131-06/CA/NCI NIH HHS/ -- T32 GM007185/GM/NIGMS NIH HHS/ -- T32 GM007185-35/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jul 30;329(5991):568-71. doi: 10.1126/science.1189992.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671189" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor/metabolism ; Cell Separation ; *Cell Transformation, Neoplastic ; Epithelial Cells/metabolism/*pathology ; Epithelium/pathology ; Flow Cytometry ; Humans ; Keratins/analysis ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Prostate/cytology/metabolism/*pathology ; Prostatic Intraepithelial Neoplasia/metabolism/*pathology ; Prostatic Neoplasms/metabolism/*pathology ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Androgen/metabolism ; Trans-Activators/metabolism ; Transduction, Genetic
    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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    Multistep synthesis of a radiolabeled imaging probe using integrated microfluidics (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-17
    Description: Microreactor technology has shown potential for optimizing synthetic efficiency, particularly in preparing sensitive compounds. We achieved the synthesis of an [(18)F]fluoride-radiolabeled molecular imaging probe, 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG), in an integrated microfluidic device. Five sequential processes-[18F]fluoride concentration, water evaporation, radiofluorination, solvent exchange, and hydrolytic deprotection-proceeded with high radio-chemical yield and purity and with shorter synthesis time relative to conventional automated synthesis. Multiple doses of [18F]FDG for positron emission tomography imaging studies in mice were prepared. These results, which constitute a proof of principle for automated multistep syntheses at the nanogram to microgram scale, could be generalized to a range of radiolabeled substrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Chung-Cheng -- Sui, Guodong -- Elizarov, Arkadij -- Shu, Chengyi Jenny -- Shin, Young-Shik -- Dooley, Alek N -- Huang, Jiang -- Daridon, Antoine -- Wyatt, Paul -- Stout, David -- Kolb, Hartmuth C -- Witte, Owen N -- Satyamurthy, Nagichettiar -- Heath, James R -- Phelps, Michael E -- Quake, Stephen R -- Tseng, Hsian-Rong -- 5T32-GM07616/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1793-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16357255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Automation ; Fluorides ; Fluorodeoxyglucose F18/*chemical synthesis ; Gas Chromatography-Mass Spectrometry ; Mice ; *Microfluidics ; Miniaturization ; Molecular Probes/*chemical synthesis ; Positron-Emission Tomography ; Radiopharmaceuticals/*chemical synthesis ; Rhabdomyosarcoma/radionuclide imaging ; Solvents ; Tomography, Emission-Computed
    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
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    Retraction (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Witte, Owen N -- Kabarowski, Janusz H -- Xu, Yan -- Le, Lu Q -- Zhu, Kui -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):206.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653487" target="_blank"〉PubMed〈/a〉
    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
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    Activation of BTK by a phosphorylation mechanism initiated by SRC family kinases (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: Bruton's tyrosine kinase (BTK) is pivotal in B cell activation and development through its participation in the signaling pathways of multiple hematopoietic receptors. The mechanisms controlling BTK activation were studied here by examination of the biochemical consequences of an interaction between BTK and SRC family kinases. This interaction of BTK with SRC kinases transphosphorylated BTK on tyrosine at residue 551, which led to BTK activation. BTK then autophosphorylated at a second site. The same two sites were phosphorylated upon B cell antigen receptor cross-linking. The activated BTK was predominantly membrane-associated, which suggests that BTK integrates distinct receptor signals resulting in SRC kinase activation and BTK membrane targeting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rawlings, D J -- Scharenberg, A M -- Park, H -- Wahl, M I -- Lin, S -- Kato, R M -- Fluckiger, A C -- Witte, O N -- Kinet, J P -- AR01912/AR/NIAMS NIH HHS/ -- AR36834/AR/NIAMS NIH HHS/ -- CA09120-20/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):822-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90095-1662, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629002" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; B-Lymphocytes/*enzymology ; Cell Line, Transformed ; Cell Membrane/enzymology ; Enzyme Activation ; Immunoglobulin M/immunology ; Lymphocyte Activation ; Mice ; Mutation ; Phosphopeptides/analysis ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/chemistry/genetics/*metabolism ; Receptors, Antigen, B-Cell/metabolism ; Signal Transduction ; src-Family Kinases/*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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  • 9
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    Differential complementation of Bcr-Abl point mutants with c-Myc (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-15
    Description: A complementation strategy was developed to define the signaling pathways activated by the Bcr-Abl tyrosine kinase. Transformation inactive point mutants of Bcr-Abl were tested for complementation with c-Myc. Single point mutations in the Src-homology 2 (SH2) domain, the major tyrosine autophosphorylation site of the kinase domain, and the Grb-2 binding site in the Bcr region impaired the transformation of fibroblasts by Bcr-Abl. Hyperexpression of c-Myc efficiently restored transformation activity only to the Bcr-Abl SH2 mutant. These data support a model in which Bcr-Abl activates at least two independent pathways for transformation. This strategy may be useful for discerning signaling pathways activated by other oncogenes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Afar, D E -- Goga, A -- McLaughlin, J -- Witte, O N -- Sawyers, C L -- CA 01551/CA/NCI NIH HHS/ -- CA 53867/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 15;264(5157):424-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California-Los Angeles 90024-1489.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8153630" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; Cell Line ; *Cell Transformation, Neoplastic ; Fusion Proteins, bcr-abl/*genetics/physiology ; GRB2 Adaptor Protein ; Gene Expression ; *Genes, abl ; *Genes, myc ; Genetic Complementation Test ; Molecular Sequence Data ; Phosphorylation ; Point Mutation ; Proteins/metabolism ; Proto-Oncogene Proteins c-myc/genetics/physiology ; Rats ; Retroviridae/physiology ; Signal Transduction ; Transfection ; Tyrosine/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Lift NIH restrictions on chimera research (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-11-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharma, Arun -- Sebastiano, Vittorio -- Scott, Christopher T -- Magnus, David -- Koyano-Nakagawa, Naoko -- Garry, Daniel J -- Witte, Owen N -- Nakauchi, Hiromitsu -- Wu, Joseph C -- Weissman, Irving L -- Wu, Sean M -- New York, N.Y. -- Science. 2015 Nov 6;350(6261):640. doi: 10.1126/science.350.6261.640-a. Epub 2015 Nov 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Center for Biomedical Ethics, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Lillehei Heart Institute, University of Minnesota, Minneapolis, MN 55455, USA. ; Lillehei Heart Institute, University of Minnesota, Minneapolis, MN 55455, USA. Stem Cell Institute and Paul and Sheila Wellstone Muscular Dystrophy Center, University of Minnesota, Minneapolis, MN 55455, USA. Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, MN 55455, USA. ; Broad Stem Cell Research Center and Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA. Center for Stem Cell Biology and Regenerative Medicine, The University of Tokyo, Tokyo, Japan. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Division of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Radiology, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA. irv@stanford.edu smwu@stanford.edu. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Division of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. irv@stanford.edu smwu@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26542560" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bioethical Issues ; Blastocyst ; *Chimera ; Financial Management/ethics ; Humans ; Mice ; National Institutes of Health (U.S.)/economics/ethics ; Pluripotent Stem Cells/*transplantation ; Stem Cell Research/economics/*ethics ; United States
    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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