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  • American Association for the Advancement of Science  (225)
  • American Association for the Advancement of Science (AAAS)  (90)
  • 1
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    Regulation of mitochondrial iron accumulation by Yfh1p, a putative homolog of frataxin (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-13
    Description: The gene responsible for Friedreich's ataxia, a disease characterized by neurodegeneration and cardiomyopathy, has recently been cloned and its product designated frataxin. A gene in Saccharomyces cerevisiae was characterized whose predicted protein product has high sequence similarity to the human frataxin protein. The yeast gene (yeast frataxin homolog, YFH1) encodes a mitochondrial protein involved in iron homeostasis and respiratory function. Human frataxin also was shown to be a mitochondrial protein. Characterizing the mechanism by which YFH1 regulates iron homeostasis in yeast may help to define the pathologic process leading to cell damage in Friedreich's ataxia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Babcock, M -- de Silva, D -- Oaks, R -- Davis-Kaplan, S -- Jiralerspong, S -- Montermini, L -- Pandolfo, M -- Kaplan, J -- DK30534/DK/NIDDK NIH HHS/ -- DK49219/DK/NIDDK NIH HHS/ -- NS34192/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1709-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, School of Medicine, University of Utah, Salt Lake City, UT 84132, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180083" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Transport ; Carrier Proteins/metabolism ; Cell Membrane/metabolism ; *Ceruloplasmin ; Cytosol/metabolism ; Friedreich Ataxia/metabolism ; Fungal Proteins/genetics/*metabolism ; Genes, Fungal ; Genetic Complementation Test ; Homeostasis ; Humans ; Iron/*metabolism ; *Iron-Binding Proteins ; Membrane Transport Proteins/metabolism ; Mitochondria/*metabolism ; Oxidative Stress ; Oxidoreductases/metabolism ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/genetics/growth & development/*metabolism ; *Saccharomyces cerevisiae Proteins ; Transformation, 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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  • 2
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    Regulation of Mitochondrial Iron Accumulation by Yfh1p, a Putative Homolog of Frataxin (1997)
    American Association for the Advancement of Science
    Details
    Publication Date: 1997-06-13
    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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    Skin Resistance Recording in the Unrestrained Rat (1962)
    American Association for the Advancement of Science
    Details
    Publication Date: 1962-12-28
    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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    Lactic Dehydrogenases: Functions of the Two Types (1964)
    American Association for the Advancement of Science
    Details
    Publication Date: 1964-02-28
    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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    Coherent single-photon emission from colloidal lead halide perovskite quantum dots (2019)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2019
    Description: 〈p〉Chemically made colloidal semiconductor quantum dots have long been proposed as scalable and color-tunable single emitters in quantum optics, but they have typically suffered from prohibitively incoherent emission. We now demonstrate that individual colloidal lead halide perovskite quantum dots (PQDs) display highly efficient single-photon emission with optical coherence times as long as 80 picoseconds, an appreciable fraction of their 210-picosecond radiative lifetimes. These measurements suggest that PQDs should be explored as building blocks in sources of indistinguishable single photons and entangled photon pairs. Our results present a starting point for the rational design of lead halide perovskite–based quantum emitters that have fast emission, wide spectral tunability, and scalable production and that benefit from the hybrid integration with nanophotonic components that has been demonstrated for colloidal materials.〈/p〉
    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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    Eight centuries of north atlantic ocean atmosphere variability (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Climate in the tropical North Atlantic is controlled largely by variations in the strength of the trade winds, the position of the Intertropical Convergence Zone, and sea surface temperatures. A high-resolution study of Caribbean sediments provides a subdecadally resolved record of tropical upwelling and trade wind variability spanning the past 825 years. These results confirm the importance of a decadal (12- to 13-year) mode of Atlantic variability believed to be driven by coupled tropical ocean-atmosphere dynamics. Although a well-defined interdecadal mode of variability does not appear to be characteristic of the tropical Atlantic, there is evidence that century-scale variability is substantial. The tropical Atlantic may also have been involved in a major shift in Northern Hemisphere climate variability that took place about 700 years ago.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Black -- Peterson -- Overpeck -- Kaplan -- Evans -- Kashgarian -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1709-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rosenstiel School of Marine and Atmospheric Science, University of Miami, Miami, FL 33149, USA. National Oceanic and Atmospheric Administration Paleoclimatology Program and the Institute for Arctic and Alpine Research, University of Colorado, B.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576732" 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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  • 7
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    An anti-apoptotic role for the p53 family member, p73, during developmental neuron death (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-15
    Description: p53 plays an essential pro-apoptotic role, a function thought to be shared with its family members p73 and p63. Here, we show that p73 is primarily present in developing neurons as a truncated isoform whose levels are dramatically decreased when sympathetic neurons apoptose after nerve growth factor (NGF) withdrawal. Increased expression of truncated p73 rescues these neurons from apoptosis induced by NGF withdrawal or p53 overexpression. In p73-/- mice, all isoforms of p73 are deleted and the apoptosis of developing sympathetic neurons is greatly enhanced. Thus, truncated p73 is an essential anti-apoptotic protein in neurons, serving to counteract the pro-apoptotic function of p53.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pozniak, C D -- Radinovic, S -- Yang, A -- McKeon, F -- Kaplan, D R -- Miller, F D -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):304-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neuronal Survival, Brain Tumor Research Center, Montreal Neurological Institute, McGill University, Montreal, Canada H3A 2B4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894779" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Apoptosis/*physiology ; Cells, Cultured ; DNA-Binding Proteins/biosynthesis/chemistry/*physiology ; Escherichia coli ; Genes, Tumor Suppressor ; Humans ; Mice ; Mice, Inbred BALB C ; Nerve Growth Factor/pharmacology ; Neurons/*physiology ; Nuclear Proteins/biosynthesis/chemistry/*physiology ; Protein Isoforms/biosynthesis/chemistry/physiology ; Recombinant Proteins ; Sympathetic Nervous System/cytology/*physiology ; Tumor Suppressor Protein p53/antagonists & inhibitors/*physiology ; Tumor Suppressor Proteins
    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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    Neurobiology. TRK makes the retrograde (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-02-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Freda D -- Kaplan, David R -- New York, N.Y. -- Science. 2002 Feb 22;295(5559):1471-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Neuronal Survival and Brain Tumor Research Centre, Montreal Neurological Institute, McGill University, 3801 rue University, Montreal, Quebec H3A 2B4, Canada. freda.miller@mcgill.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11859179" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Cell Survival ; Enzyme Activation ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases/metabolism ; Models, Neurological ; Nerve Growth Factor/*metabolism ; Neurons/metabolism/*physiology ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Transport ; Rats ; Receptor, trkA/*metabolism ; *Signal Transduction ; Transport Vesicles/metabolism
    Print ISSN: 0036-8075
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  • 9
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    Management accounting for advanced technological environments (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-08-25
    Description: Management accounting systems designed decades ago no longer provide timely, relevant information for companies in today's highly competitive environment. New operational control and performance measurement systems are recognizing the importance of direct measurement of quality, manufacturing lead times, flexibility, and customer responsiveness, as well as more accurate measures of the actual costs of consumed resources. Activity-based cost systems can assign the costs of indirect and support resources to the specific products and activities that benefit from these resources. Both operational control and activity-based systems represent new opportunities for improved managerial information in complex, technologically advanced environments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaplan, R S -- New York, N.Y. -- Science. 1989 Aug 25;245(4920):819-23.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17773356" target="_blank"〉PubMed〈/a〉
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  • 10
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    Direct regulation of the Akt proto-oncogene product by phosphatidylinositol-3,4-bisphosphate (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-31
    Description: The regulation of the serine-threonine kinase Akt by lipid products of phosphoinositide 3-kinase (PI 3-kinase) was investigated. Akt activity was found to correlate with the amount of phosphatidylinositol-3,4-bisphosphate (PtdIns-3,4-P2) in vivo, and synthetic PtdIns-3,4-P2 activated Akt both in vitro and in vivo. Binding of PtdIns-3,4-P2 occurred within the Akt pleckstrin homology (PH) domain and facilitated dimerization of Akt. Akt mutated in the PH domain was not activated by PI 3-kinase in vivo or by PtdIns-3, 4-P2 in vitro, and it was impaired in binding to PtdIns-3,4-P2. Examination of the binding to other phosphoinositides revealed that they bound to the Akt PH domain with much lower affinity than did PtdIns-3,4-P2 and failed to increase Akt activity. Thus, Akt is apparently regulated by the direct interaction of PtdIns-3,4-P2 with the Akt PH domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Franke, T F -- Kaplan, D R -- Cantley, L C -- Toker, A -- GM41890/GM/NIGMS NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- R01 GM041890/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):665-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research Facility and Development Center (NCI-FCRFDC), Frederick, MD 21702, USA. tfranke@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005852" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; COS Cells ; Dimerization ; Enzyme Activation ; Mice ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositol Phosphates/*metabolism/pharmacology ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Platelet-Derived Growth Factor/pharmacology ; Point Mutation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-akt ; Recombinant Fusion Proteins/chemistry/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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