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  • Cell Press  (42)
  • Nature Publishing Group (NPG)
  • 2010-2014  (42)
  • 2000-2004  (12)
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  • 1
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    Patterning of the Dorsal Telencephalon and Cerebral Cortex by a Roof Plate-Lhx2 Pathway (2001)
    Cell Press
    Details
    Publication Date: 2001-11-01
    Print ISSN: 0896-6273
    Electronic ISSN: 1097-4199
    Topics: Biology , Medicine
    Published by Cell Press
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  • 2
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    Differential Recruitment of the Sensorimotor Putamen and Frontoparietal Cortex during Motor Chunking in Humans (2012)
    Cell Press
    Details
    Publication Date: 2012-06-01
    Print ISSN: 0896-6273
    Electronic ISSN: 1097-4199
    Topics: Biology , Medicine
    Published by Cell Press
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  • 3
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    Hippocampal Representation of Related and Opposing Memories Develop within Distinct, Hierarchically Organized Neural Schemas (2014)
    Cell Press
    Details
    Publication Date: 2014-07-01
    Print ISSN: 0896-6273
    Electronic ISSN: 1097-4199
    Topics: Biology , Medicine
    Published by Cell Press
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  • 4
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    The landscape of somatic copy-number alteration across human cancers (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-02-19
    Description: A powerful way to discover key genes with causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. Here we present high-resolution analyses of somatic copy-number alterations (SCNAs) from 3,131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across several cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several gene families are enriched among these regions of focal SCNA, including the BCL2 family of apoptosis regulators and the NF-kappaBeta pathway. We show that cancer cells containing amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend on the expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in several cancer types.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2826709/" 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/PMC2826709/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beroukhim, Rameen -- Mermel, Craig H -- Porter, Dale -- Wei, Guo -- Raychaudhuri, Soumya -- Donovan, Jerry -- Barretina, Jordi -- Boehm, Jesse S -- Dobson, Jennifer -- Urashima, Mitsuyoshi -- Mc Henry, Kevin T -- Pinchback, Reid M -- Ligon, Azra H -- Cho, Yoon-Jae -- Haery, Leila -- Greulich, Heidi -- Reich, Michael -- Winckler, Wendy -- Lawrence, Michael S -- Weir, Barbara A -- Tanaka, Kumiko E -- Chiang, Derek Y -- Bass, Adam J -- Loo, Alice -- Hoffman, Carter -- Prensner, John -- Liefeld, Ted -- Gao, Qing -- Yecies, Derek -- Signoretti, Sabina -- Maher, Elizabeth -- Kaye, Frederic J -- Sasaki, Hidefumi -- Tepper, Joel E -- Fletcher, Jonathan A -- Tabernero, Josep -- Baselga, Jose -- Tsao, Ming-Sound -- Demichelis, Francesca -- Rubin, Mark A -- Janne, Pasi A -- Daly, Mark J -- Nucera, Carmelo -- Levine, Ross L -- Ebert, Benjamin L -- Gabriel, Stacey -- Rustgi, Anil K -- Antonescu, Cristina R -- Ladanyi, Marc -- Letai, Anthony -- Garraway, Levi A -- Loda, Massimo -- Beer, David G -- True, Lawrence D -- Okamoto, Aikou -- Pomeroy, Scott L -- Singer, Samuel -- Golub, Todd R -- Lander, Eric S -- Getz, Gad -- Sellers, William R -- Meyerson, Matthew -- K08 AR055688/AR/NIAMS NIH HHS/ -- K08 AR055688-03/AR/NIAMS NIH HHS/ -- K08 AR055688-04/AR/NIAMS NIH HHS/ -- K08 CA122833/CA/NCI NIH HHS/ -- K08 CA122833-01A1/CA/NCI NIH HHS/ -- K08 CA122833-02/CA/NCI NIH HHS/ -- K08 CA122833-03/CA/NCI NIH HHS/ -- K08 CA134931/CA/NCI NIH HHS/ -- K08CA122833/CA/NCI NIH HHS/ -- P01CA 098101/CA/NCI NIH HHS/ -- P01CA085859/CA/NCI NIH HHS/ -- P50CA90578/CA/NCI NIH HHS/ -- R01 CA109038/CA/NCI NIH HHS/ -- R01 GM074024/GM/NIGMS NIH HHS/ -- R01CA109038/CA/NCI NIH HHS/ -- R01CA109467/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- U24 CA126546/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Feb 18;463(7283):899-905. doi: 10.1038/nature08822.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Program and Medical and Population Genetics Group, The Broad Institute of M.I.T. and Harvard, 7 Cambridge Center.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20164920" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis/genetics ; Cell Line, Tumor ; Cell Survival/genetics ; DNA Copy Number Variations/*genetics ; Gene Amplification/genetics ; Gene Dosage/*genetics ; Genomics ; Humans ; Multigene Family/genetics ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasms/classification/*genetics/pathology ; Proto-Oncogene Proteins c-bcl-2/genetics ; Signal Transduction ; bcl-X Protein/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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  • 5
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    The Rubisco enzyme and agricultural productivity (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porter, John R -- Wollenweber, Bernd -- England -- Nature. 2010 Feb 18;463(7283):876. doi: 10.1038/463876b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20164901" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/*methods ; Crops, Agricultural/genetics/*growth & development/metabolism ; *Food Supply/statistics & numerical data ; Food, Genetically Modified ; *Genetic Engineering ; Ribulose-Bisphosphate Carboxylase/genetics/*metabolism
    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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  • 6
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    How will growing cities eat? (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-01-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porter, John R -- Deutsch, Lisa -- Dumaresq, David -- Dyball, Rob -- England -- Nature. 2011 Jan 6;469(7328):34. doi: 10.1038/469034d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21209650" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/statistics & numerical data/*trends ; Cities/*statistics & numerical data ; Food Supply/*statistics & numerical data ; *Population Growth ; Urban Population/*statistics & numerical data/trends
    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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  • 7
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    An unexpectedly low oscillator strength as the origin of the Fe XVII emission problem (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-12-14
    Description: Highly charged iron (Fe(16+), here referred to as Fe XVII) produces some of the brightest X-ray emission lines from hot astrophysical objects, including galaxy clusters and stellar coronae, and it dominates the emission of the Sun at wavelengths near 15 angstroms. The Fe XVII spectrum is, however, poorly fitted by even the best astrophysical models. A particular problem has been that the intensity of the strongest Fe XVII line is generally weaker than predicted. This has affected the interpretation of observations by the Chandra and XMM-Newton orbiting X-ray missions, fuelling a continuing controversy over whether this discrepancy is caused by incomplete modelling of the plasma environment in these objects or by shortcomings in the treatment of the underlying atomic physics. Here we report the results of an experiment in which a target of iron ions was induced to fluoresce by subjecting it to femtosecond X-ray pulses from a free-electron laser; our aim was to isolate a key aspect of the quantum mechanical description of the line emission. Surprisingly, we find a relative oscillator strength that is unexpectedly low, differing by 3.6sigma from the best quantum mechanical calculations. Our measurements suggest that the poor agreement is rooted in the quality of the underlying atomic wavefunctions rather than in insufficient modelling of collisional processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bernitt, S -- Brown, G V -- Rudolph, J K -- Steinbrugge, R -- Graf, A -- Leutenegger, M -- Epp, S W -- Eberle, S -- Kubicek, K -- Mackel, V -- Simon, M C -- Trabert, E -- Magee, E W -- Beilmann, C -- Hell, N -- Schippers, S -- Muller, A -- Kahn, S M -- Surzhykov, A -- Harman, Z -- Keitel, C H -- Clementson, J -- Porter, F S -- Schlotter, W -- Turner, J J -- Ullrich, J -- Beiersdorfer, P -- Lopez-Urrutia, J R Crespo -- England -- Nature. 2012 Dec 13;492(7428):225-8. doi: 10.1038/nature11627.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Kernphysik, 69117 Heidelberg, Germany. sven.bernitt@mpi-hd.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23235875" target="_blank"〉PubMed〈/a〉
    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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    De novo mutations in histone-modifying genes in congenital heart disease (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-05-15
    Description: Congenital heart disease (CHD) is the most frequent birth defect, affecting 0.8% of live births. Many cases occur sporadically and impair reproductive fitness, suggesting a role for de novo mutations. Here we compare the incidence of de novo mutations in 362 severe CHD cases and 264 controls by analysing exome sequencing of parent-offspring trios. CHD cases show a significant excess of protein-altering de novo mutations in genes expressed in the developing heart, with an odds ratio of 7.5 for damaging (premature termination, frameshift, splice site) mutations. Similar odds ratios are seen across the main classes of severe CHD. We find a marked excess of de novo mutations in genes involved in the production, removal or reading of histone 3 lysine 4 (H3K4) methylation, or ubiquitination of H2BK120, which is required for H3K4 methylation. There are also two de novo mutations in SMAD2, which regulates H3K27 methylation in the embryonic left-right organizer. The combination of both activating (H3K4 methylation) and inactivating (H3K27 methylation) chromatin marks characterizes 'poised' promoters and enhancers, which regulate expression of key developmental genes. These findings implicate de novo point mutations in several hundreds of genes that collectively contribute to approximately 10% of severe CHD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3706629/" 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/PMC3706629/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zaidi, Samir -- Choi, Murim -- Wakimoto, Hiroko -- Ma, Lijiang -- Jiang, Jianming -- Overton, John D -- Romano-Adesman, Angela -- Bjornson, Robert D -- Breitbart, Roger E -- Brown, Kerry K -- Carriero, Nicholas J -- Cheung, Yee Him -- Deanfield, John -- DePalma, Steve -- Fakhro, Khalid A -- Glessner, Joseph -- Hakonarson, Hakon -- Italia, Michael J -- Kaltman, Jonathan R -- Kaski, Juan -- Kim, Richard -- Kline, Jennie K -- Lee, Teresa -- Leipzig, Jeremy -- Lopez, Alexander -- Mane, Shrikant M -- Mitchell, Laura E -- Newburger, Jane W -- Parfenov, Michael -- Pe'er, Itsik -- Porter, George -- Roberts, Amy E -- Sachidanandam, Ravi -- Sanders, Stephan J -- Seiden, Howard S -- State, Mathew W -- Subramanian, Sailakshmi -- Tikhonova, Irina R -- Wang, Wei -- Warburton, Dorothy -- White, Peter S -- Williams, Ismee A -- Zhao, Hongyu -- Seidman, Jonathan G -- Brueckner, Martina -- Chung, Wendy K -- Gelb, Bruce D -- Goldmuntz, Elizabeth -- Seidman, Christine E -- Lifton, Richard P -- 5U54HG006504/HG/NHGRI NIH HHS/ -- F30 HL123238/HL/NHLBI NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- T32 GM007205/GM/NIGMS NIH HHS/ -- U01 HG006546/HG/NHGRI NIH HHS/ -- U01 HL098123/HL/NHLBI NIH HHS/ -- U01 HL098147/HL/NHLBI NIH HHS/ -- U01 HL098153/HL/NHLBI NIH HHS/ -- U01 HL098162/HL/NHLBI NIH HHS/ -- U01 HL098163/HL/NHLBI NIH HHS/ -- U01-HL098123/HL/NHLBI NIH HHS/ -- U01-HL098147/HL/NHLBI NIH HHS/ -- U01-HL098153/HL/NHLBI NIH HHS/ -- U01-HL098162/HL/NHLBI NIH HHS/ -- U01-HL098163/HL/NHLBI NIH HHS/ -- U01-HL098188/HL/NHLBI NIH HHS/ -- U54 HG006504/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jun 13;498(7453):220-3. doi: 10.1038/nature12141. Epub 2013 May 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Yale University School of Medicine, New Haven, Connecticut 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23665959" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Case-Control Studies ; Child ; Chromatin/chemistry/metabolism ; DNA Mutational Analysis ; Enhancer Elements, Genetic/genetics ; Exome/genetics ; Female ; Genes, Developmental/genetics ; Heart Diseases/*congenital/*genetics/metabolism ; Histones/chemistry/*metabolism ; Humans ; Lysine/chemistry/metabolism ; Male ; Methylation ; Mutation ; Odds Ratio ; Promoter Regions, Genetic/genetics
    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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    National carbon stocks: Move on to a carbon currency standard (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-02-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porter, John R -- Wratten, Steve -- England -- Nature. 2014 Feb 20;506(7488):295. doi: 10.1038/506295a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Copenhagen, Denmark. ; Lincoln University, New Zealand.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24553231" target="_blank"〉PubMed〈/a〉
    Keywords: Gross Domestic Product/*trends ; Humans ; *Quality of Life ; Sociology/*methods
    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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    Dauer-independent insulin/IGF-1-signalling implicates collagen remodelling in longevity (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-12-18
    Description: Interventions that delay ageing mobilize mechanisms that protect and repair cellular components, but it is unknown how these interventions might slow the functional decline of extracellular matrices, which are also damaged during ageing. Reduced insulin/IGF-1 signalling (rIIS) extends lifespan across the evolutionary spectrum, and in juvenile Caenorhabditis elegans also allows the transcription factor DAF-16/FOXO to induce development into dauer, a diapause that withstands harsh conditions. It has been suggested that rIIS delays C. elegans ageing through activation of dauer-related processes during adulthood, but some rIIS conditions confer robust lifespan extension unaccompanied by any dauer-like traits. Here we show that rIIS can promote C. elegans longevity through a program that is genetically distinct from the dauer pathway, and requires the Nrf (NF-E2-related factor) orthologue SKN-1 acting in parallel to DAF-16. SKN-1 is inhibited by IIS and has been broadly implicated in longevity, but is rendered dispensable for rIIS lifespan extension by even mild activity of dauer-related processes. When IIS is decreased under conditions that do not induce dauer traits, SKN-1 most prominently increases expression of collagens and other extracellular matrix genes. Diverse genetic, nutritional, and pharmacological pro-longevity interventions delay an age-related decline in collagen expression. These collagens mediate adulthood extracellular matrix remodelling, and are needed for ageing to be delayed by interventions that do not involve dauer traits. By genetically delineating a dauer-independent rIIS ageing pathway, our results show that IIS controls a broad set of protective mechanisms during C. elegans adulthood, and may facilitate elucidation of processes of general importance for longevity. The importance of collagen production in diverse anti-ageing interventions implies that extracellular matrix remodelling is a generally essential signature of longevity assurance, and that agents promoting extracellular matrix youthfulness may have systemic benefit.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352135/" 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/PMC4352135/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ewald, Collin Y -- Landis, Jess N -- Porter Abate, Jess -- Murphy, Coleen T -- Blackwell, T Keith -- 5T32DK007260/DK/NIDDK NIH HHS/ -- GM062891/GM/NIGMS NIH HHS/ -- P30 DK036836/DK/NIDDK NIH HHS/ -- P30DK036836/DK/NIDDK NIH HHS/ -- R01 GM062891/GM/NIGMS NIH HHS/ -- England -- Nature. 2015 Mar 5;519(7541):97-101. doi: 10.1038/nature14021. Epub 2014 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Joslin Diabetes Center, One Joslin Place, Boston, Massachusetts 02215, USA [2] Harvard Stem Cell Institute, 7 Divinity Avenue, Cambridge, Massachusetts 02138, USA [3] Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02215, USA. ; Department of Molecular Biology, Lewis-Sigler Institute for Integrative Genomics, Princeton University, 148 Carl Icahn Laboratory, Washington Road, Princeton, New Jersey 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25517099" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Animals ; Caenorhabditis elegans/growth & development/*metabolism ; Caenorhabditis elegans Proteins/*metabolism ; Collagen/biosynthesis/genetics/*metabolism ; DNA-Binding Proteins/*metabolism ; Extracellular Matrix/metabolism ; Forkhead Transcription Factors ; Insulin/*metabolism ; Insulin-Like Growth Factor I/*metabolism ; Larva/growth & development ; Longevity/*physiology ; *Signal Transduction ; Transcription Factors/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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