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  • Humans  (10)
  • Earthquake  (4)
  • ASTROPHYSICS  (3)
  • 2005-2009  (12)
  • 1990-1994  (5)
  • 1
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    Generation of transgenic non-human primates with germline transmission (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-05-30
    Description: The common marmoset (Callithrix jacchus) is increasingly attractive for use as a non-human primate animal model in biomedical research. It has a relatively high reproduction rate for a primate, making it potentially suitable for transgenic modification. Although several attempts have been made to produce non-human transgenic primates, transgene expression in the somatic tissues of live infants has not been demonstrated by objective analyses such as polymerase chain reaction with reverse transcription or western blots. Here we show that the injection of a self-inactivating lentiviral vector in sucrose solution into marmoset embryos results in transgenic common marmosets that expressed the transgene in several organs. Notably, we achieved germline transmission of the transgene, and the transgenic offspring developed normally. The successful creation of transgenic marmosets provides a new animal model for human disease that has the great advantage of a close genetic relationship with humans. This model will be valuable to many fields of biomedical research.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sasaki, Erika -- Suemizu, Hiroshi -- Shimada, Akiko -- Hanazawa, Kisaburo -- Oiwa, Ryo -- Kamioka, Michiko -- Tomioka, Ikuo -- Sotomaru, Yusuke -- Hirakawa, Reiko -- Eto, Tomoo -- Shiozawa, Seiji -- Maeda, Takuji -- Ito, Mamoru -- Ito, Ryoji -- Kito, Chika -- Yagihashi, Chie -- Kawai, Kenji -- Miyoshi, Hiroyuki -- Tanioka, Yoshikuni -- Tamaoki, Norikazu -- Habu, Sonoko -- Okano, Hideyuki -- Nomura, Tatsuji -- England -- Nature. 2009 May 28;459(7246):523-7. doi: 10.1038/nature08090.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Central Institute for Experimental Animals, 1430 Nogawa, Miyamae-ku, Kawasaki, Kanagawa 216-0001, Japan. esasaki@ciea.or.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478777" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified/*genetics ; Animals, Newborn ; Callithrix/embryology/*genetics ; *Disease Models, Animal ; Gene Expression Profiling ; Germ Cells/*metabolism ; Green Fluorescent Proteins/genetics ; Heredity/*genetics ; Humans ; Transcription, Genetic ; Transgenes/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    alpha-Klotho as a regulator of calcium homeostasis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-16
    Description: alpha-klotho was identified as a gene associated with premature aging-like phenotypes characterized by short lifespan. In mice, we found the molecular association of alpha-Klotho (alpha-Kl) and Na+,K+-adenosine triphosphatase (Na+,K+-ATPase) and provide evidence for an increase of abundance of Na+,K+-ATPase at the plasma membrane. Low concentrations of extracellular free calcium ([Ca2+]e) rapidly induce regulated parathyroid hormone (PTH) secretion in an alpha-Kl- and Na+,K+-ATPase-dependent manner. The increased Na+ gradient created by Na+,K+-ATPase activity might drive the transepithelial transport of Ca2+ in cooperation with ion channels and transporters in the choroid plexus and the kidney. Our findings reveal fundamental roles of alpha-Kl in the regulation of calcium metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imura, Akihiro -- Tsuji, Yoshihito -- Murata, Miyahiko -- Maeda, Ryota -- Kubota, Koji -- Iwano, Akiko -- Obuse, Chikashi -- Togashi, Kazuya -- Tominaga, Makoto -- Kita, Naoko -- Tomiyama, Ken-ichi -- Iijima, Junko -- Nabeshima, Yoko -- Fujioka, Makio -- Asato, Ryo -- Tanaka, Shinzo -- Kojima, Ken -- Ito, Juichi -- Nozaki, Kazuhiko -- Hashimoto, Nobuo -- Ito, Tetsufumi -- Nishio, Takeshi -- Uchiyama, Takashi -- Fujimori, Toshihiko -- Nabeshima, Yo-ichi -- New York, N.Y. -- Science. 2007 Jun 15;316(5831):1615-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17569864" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/cerebrospinal fluid/*metabolism ; Cell Membrane/enzymology/metabolism ; Choroid Plexus/metabolism ; Cytoplasm/enzymology/metabolism ; Endoplasmic Reticulum/metabolism ; Endosomes/metabolism ; Enzyme Inhibitors/pharmacology ; Feedback, Physiological ; Glucuronidase/genetics/metabolism/*physiology ; Golgi Apparatus/metabolism ; HeLa Cells ; *Homeostasis ; Humans ; Ion Transport ; Kidney/enzymology/metabolism ; Mice ; Ouabain/pharmacology ; Parathyroid Glands/enzymology/metabolism ; Parathyroid Hormone/secretion ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors/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)
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  • 3
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    Heat signature on the Chelungpu fault associated with the 1999 Chi-Chi, Taiwan earthquake (2006)
    In:  Geophys. Res. Lett., Amsterdam, Elsevier Scientific Publishing Company, vol. 33, no. 14, pp. 879-897, pp. L14306, (ISSN: 1340-4202)
    Details
    Publication Date: 2006
    Keywords: Geothermics ; Friction ; Fault zone ; China ; Earthquake ; GRL ; 5134 ; Physical ; Properties ; of ; Rocks: ; Thermal ; properties ; 7209 ; Seismology: ; Earthquake ; dynamics ; (1242) ; 8130 ; Tectonophysics: ; Heat ; generation ; and ; transport ; 8163 ; Rheology ; and ; friction ; of ; fault ; zones ; (8034)
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    BIBLIOGRAPHY SEISMOLOGY
  • 4
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    Very low frequency earthquakes within accretionary prisms are very low stress-drop earthquakes (2006)
    In:  Geophys. Res. Lett., Amsterdam, Schweizerbart'sche Verlagsbuchhandlung, vol. 33, no. 9, pp. 1-4, pp. L09302, (ISSN 0016-8548, ISBN 3-510-50045-8)
    Details
    Publication Date: 2006
    Keywords: red ; slow ; silent ; Earthquake ; Subduction zone ; Stress drop ; Seismology ; GRL ; 7203 ; Seismology: ; Body ; waves ; 7215 ; Earthquake ; source ; observations ; 7240 ; Subduction ; zones ; 8118 ; Tectonophysics: ; Dynamics ; and ; mechanics ; of ; faulting ; 8170 ; Subduction ; zone ; processes
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    BIBLIOGRAPHY SEISMOLOGY
  • 5
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    Did expanded porous patches guide rupture propagation in 2003 Tokachi-oki earthquake? (2005)
    In:  Geophys. Res. Lett., Taipei, EGS, vol. 32, no. 20, pp. 105-121, pp. L20310, (ISSN: 1340-4202)
    Details
    Publication Date: 2005
    Keywords: Deep seismic sounding (espec. cont. crust) ; Reflection seismics ; 4D ; Aftershocks ; Earthquake asperities ; Fracture ; Earthquake ; Seismology ; Rock mechanics ; Physical properties of rocks ; GRL ; 3225 ; Mathematical ; Geophysics: ; Numerical ; approximations ; and ; analysis ; (4260) ; 3653 ; Mineralogy ; and ; Petrology: ; Fluid ; flow ; 7230 ; Seismology: ; Seismicity ; and ; tectonics ; (1207, ; 1217, ; 1240, ; 1242) ; 7240 ; Subduction ; zones ; (1207, ; 1219, ; 1240)
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  • 6
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    Source fault structure of the 2003 Bam earthquake, southeastern Iran, inferred from the aftershock distribution and its relation to the heavily damaged area: Existence of the Arg-e-Bam fault proposed (2005)
    In:  Geophys. Res. Lett., Colorado Springs, US Air Force Academy, vol. 32, no. 9, pp. 389-398, pp. L09308, (ISSN: 1340-4202)
    Details
    Publication Date: 2005
    Keywords: Earthquake ; Aftershocks ; Source parameters ; Fault zone ; GRL
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    BIBLIOGRAPHY SEISMOLOGY
  • 7
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    PML targeting eradicates quiescent leukaemia-initiating cells (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-05-13
    Description: The existence of a small population of 'cancer-initiating cells' responsible for tumour maintenance has been firmly demonstrated in leukaemia. This concept is currently being tested in solid tumours. Leukaemia-initiating cells, particularly those that are in a quiescent state, are thought to be resistant to chemotherapy and targeted therapies, resulting in disease relapse. Chronic myeloid leukaemia is a paradigmatic haematopoietic stem cell disease in which the leukaemia-initiating-cell pool is not eradicated by current therapy, leading to disease relapse on drug discontinuation. Here we define the critical role of the promyelocytic leukaemia protein (PML) tumour suppressor in haematopoietic stem cell maintenance, and present a new therapeutic approach for targeting quiescent leukaemia-initiating cells and possibly cancer-initiating cells by pharmacological inhibition of PML.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712082/" 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/PMC2712082/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Keisuke -- Bernardi, Rosa -- Morotti, Alessandro -- Matsuoka, Sahoko -- Saglio, Giuseppe -- Ikeda, Yasuo -- Rosenblatt, Jacalyn -- Avigan, David E -- Teruya-Feldstein, Julie -- Pandolfi, Pier Paolo -- K99 CA139009/CA/NCI NIH HHS/ -- R00 CA139009/CA/NCI NIH HHS/ -- R37 CA071692/CA/NCI NIH HHS/ -- R37 CA071692-12/CA/NCI NIH HHS/ -- England -- Nature. 2008 Jun 19;453(7198):1072-8. doi: 10.1038/nature07016. Epub 2008 May 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genetics Program, Beth Israel Deaconess Cancer Center, Department of Medicine, Harvard Medical School, New Research Building, 330 Brookline Avenue, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18469801" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Arsenicals/pharmacology/therapeutic use ; Cell Line ; Coculture Techniques ; Female ; Gene Expression Regulation, Neoplastic ; Hematopoietic Stem Cells/pathology ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism/*pathology ; Male ; Mice ; Mice, Inbred C57BL ; Neoplastic Stem Cells/metabolism/*pathology ; Nuclear Proteins/antagonists & inhibitors/deficiency/genetics/*metabolism ; Oxides/pharmacology/therapeutic use ; Recurrence ; Regeneration ; Transcription Factors/antagonists & inhibitors/deficiency/genetics/*metabolism ; Tumor Suppressor Proteins/antagonists & ; inhibitors/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Big data: the next Google. Interview by Duncan Graham-Rowe (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-09-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buxton, Bill -- Hayward, Vincent -- Pearson, Ian -- Karkkainen, Leo -- Greiner, Helen -- Dyson, Esther -- Ito, Joi -- Chung, Anshe -- Kelly, Kevin -- Schillace, Sam -- England -- Nature. 2008 Sep 4;455(7209):8-9. doi: 10.1038/455008a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18769400" target="_blank"〉PubMed〈/a〉
    Keywords: Computer Graphics/trends ; Electronics/trends ; Genetic Predisposition to Disease ; Humans ; Internet/*trends ; Records as Topic ; Robotics/trends ; Touch ; User-Computer Interface
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Developmental and species-divergent globin switching are driven by BCL11A (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-08-07
    Description: The contribution of changes in cis-regulatory elements or trans-acting factors to interspecies differences in gene expression is not well understood. The mammalian beta-globin loci have served as a model for gene regulation during development. Transgenic mice containing the human beta-globin locus, consisting of the linked embryonic (epsilon), fetal (gamma) and adult (beta) genes, have been used as a system to investigate the temporal switch from fetal to adult haemoglobin, as occurs in humans. Here we show that the human gamma-globin (HBG) genes in these mice behave as murine embryonic globin genes, revealing a limitation of the model and demonstrating that critical differences in the trans-acting milieu have arisen during mammalian evolution. We show that the expression of BCL11A, a repressor of human gamma-globin expression identified by genome-wide association studies, differs between mouse and human. Developmental silencing of the mouse embryonic globin and human gamma-globin genes fails to occur in mice in the absence of BCL11A. Thus, BCL11A is a critical mediator of species-divergent globin switching. By comparing the ontogeny of beta-globin gene regulation in mice and humans, we have shown that alterations in the expression of a trans-acting factor constitute a critical driver of gene expression changes during evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749913/" 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/PMC3749913/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sankaran, Vijay G -- Xu, Jian -- Ragoczy, Tobias -- Ippolito, Gregory C -- Walkley, Carl R -- Maika, Shanna D -- Fujiwara, Yuko -- Ito, Masafumi -- Groudine, Mark -- Bender, M A -- Tucker, Philip W -- Orkin, Stuart H -- P01 HL032262/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Aug 27;460(7259):1093-7. doi: 10.1038/nature08243. Epub 2009 Aug 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Children's Hospital Boston and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19657335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/*metabolism ; Embryo, Mammalian/metabolism ; Evolution, Molecular ; Fetus/metabolism ; *Gene Expression Regulation, Developmental ; Gene Silencing ; Globins/*genetics ; Hematopoiesis ; Humans ; Mice ; Nuclear Proteins/genetics/*metabolism ; Species Specificity ; beta-Globins/genetics ; gamma-Globins/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    GlcNAcylation of a histone methyltransferase in retinoic-acid-induced granulopoiesis (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-04-21
    Description: The post-translational modifications of histone tails generate a 'histone code' that defines local and global chromatin states. The resultant regulation of gene function is thought to govern cell fate, proliferation and differentiation. Reversible histone modifications such as methylation are under mutual controls to organize chromosomal events. Among the histone modifications, methylation of specific lysine and arginine residues seems to be critical for chromatin configuration and control of gene expression. Methylation of histone H3 lysine 4 (H3K4) changes chromatin into a transcriptionally active state. Reversible modification of proteins by beta-N-acetylglucosamine (O-GlcNAc) in response to serum glucose levels regulates diverse cellular processes. However, the epigenetic impact of protein GlcNAcylation is unknown. Here we report that nuclear GlcNAcylation of a histone lysine methyltransferase (HKMT), MLL5, by O-GlcNAc transferase facilitates retinoic-acid-induced granulopoiesis in human HL60 promyelocytes through methylation of H3K4. MLL5 is biochemically identified in a GlcNAcylation-dependent multi-subunit complex associating with nuclear retinoic acid receptor RARalpha (also known as RARA), serving as a mono- and di-methyl transferase to H3K4. GlcNAcylation at Thr 440 in the MLL5 SET domain evokes its H3K4 HKMT activity and co-activates RARalpha in target gene promoters. Increased nuclear GlcNAcylation by means of O-GlcNAc transferase potentiates retinoic-acid-induced HL60 granulopoiesis and restores the retinoic acid response in the retinoic-acid-resistant HL60-R2 cell line. Thus, nuclear MLL5 GlcNAcylation triggers cell lineage determination of HL60 through activation of its HKMT activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujiki, Ryoji -- Chikanishi, Toshihiro -- Hashiba, Waka -- Ito, Hiroaki -- Takada, Ichiro -- Roeder, Robert G -- Kitagawa, Hirochika -- Kato, Shigeaki -- England -- Nature. 2009 May 21;459(7245):455-9. doi: 10.1038/nature07954. Epub 2009 Apr 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19377461" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylglucosamine/*metabolism ; Cell Lineage ; Cell Nucleus/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Granulocytes/*cytology/*drug effects ; HL-60 Cells ; Histone-Lysine N-Methyltransferase/chemistry/*metabolism ; Humans ; Leukopoiesis/*drug effects ; Multiprotein Complexes/chemistry/isolation & purification/metabolism ; N-Acetylglucosaminyltransferases/chemistry/*metabolism ; Protein Structure, Tertiary ; Receptors, Retinoic Acid/metabolism ; Threonine/metabolism ; Tretinoin/*pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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