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  • Articles  (13)
  • Animals  (13)
  • D63
  • Polymer and Materials Science
  • Science. 209(4455): 510-3.  (1)
  • Science. 217(4561): 743-5.  (1)
  • Science. 258(5084): 1004-7.  (1)
  • Science. 264(5164): 1415-21.  (1)
  • Science. 267(5202): 1347-9.  (1)
  • Science. 273(5276): 750-1.  (1)
  • Science. 279(5354): 1216-9.  (1)
  • Science. 312(5780): 1659-62. doi: 10.1126/science.1127233.  (1)
  • Science. 314(5801): 923-4.  (1)
  • Science. 322(5906): 1387-92. doi: 10.1126/science.1165171.  (1)
  • Science. 327(5961): 84-7. doi: 10.1126/science.1180616.  (1)
  • Science. 339(6123): 1074-7. doi: 10.1126/science.1232542.  (1)
  • Science. 352(6284): 459-63. doi: 10.1126/science.aad2035.  (1)
  • 25
  • Biology  (13)
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  • Articles  (13)
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  • 1
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    Mass spectrometric analysis of the anaphase-promoting complex from yeast: identification of a subunit related to cullins (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: Entry into anaphase and exit from mitosis depend on a ubiquitin-protein ligase complex called the anaphase-promoting complex (APC) or cyclosome. At least 12 different subunits were detected in the purified particle from budding yeast, including the previously identified proteins Apc1p, Cdc16p, Cdc23p, Cdc26p, and Cdc27p. Five additional subunits purified in low nanogram amounts were identified by tandem mass spectrometric sequencing. Apc2p, Apc5p, and the RING-finger protein Apc11p are conserved from yeast to humans. Apc2p is similar to the cullin Cdc53p, which is a subunit of the ubiquitin-protein ligase complex SCFCdc4 required for the initiation of DNA replication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zachariae, W -- Shevchenko, A -- Andrews, P D -- Ciosk, R -- Galova, M -- Stark, M J -- Mann, M -- Nasmyth, K -- New York, N.Y. -- Science. 1998 Feb 20;279(5354):1216-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology, Dr. Bohr-Gasse 7, A-1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9469814" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Anaphase ; Anaphase-Promoting Complex-Cyclosome ; Animals ; Cell Cycle Proteins/chemistry/metabolism ; *Cullin Proteins ; Cyclins/metabolism ; DNA Replication ; Fungal Proteins/*chemistry/genetics/isolation & purification ; Genes, Fungal ; Humans ; Ligases/*chemistry/genetics/isolation & purification ; Mass Spectrometry ; Molecular Sequence Data ; Saccharomyces cerevisiae/*chemistry/*cytology/genetics ; *Saccharomyces cerevisiae Proteins ; Sequence Alignment ; Spindle Apparatus/metabolism ; *Ubiquitin-Protein Ligase Complexes ; Ubiquitin-Protein Ligases ; Ubiquitins/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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  • 2
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    A surface protease and the invasive character of plague (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-06
    Description: A 9.5-kilobase plasmid of Yersinia pestis, the causative agent of plague, is required for high virulence when mice are inoculated with the bacterium by subcutaneous injection. Inactivation of the plasmid gene pla, which encodes a surface protease, increased the median lethal dose of the bacteria for mice by a millionfold. Moreover, cloned pla was sufficient to restore segregants lacking the entire pla-bearing plasmid to full virulence. Both pla+ strains injected subcutaneously and pla- mutants injected intravenously reached high titers in liver and spleen of infected mice, whereas pla- mutants injected subcutaneously failed to do so even though they establish a sustained local infection at the injection site. More inflammatory cells accumulated in lesions caused by the pla- mutants than in lesions produced by the pla+ parent. The Pla protease was shown to be a plasminogen activator with unusual kinetic properties. It can also cleave complement C3 at a specific site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sodeinde, O A -- Subrahmanyam, Y V -- Stark, K -- Quan, T -- Bao, Y -- Goguen, J D -- AI22176/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 6;258(5084):1004-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester 01655.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439793" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Bacterial Proteins ; Colony Count, Microbial ; Escherichia coli/enzymology ; Fibrinolysin/chemistry/metabolism ; Injections, Intravenous ; Kinetics ; Liver/microbiology ; Mice ; Molecular Sequence Data ; Mutation ; Plague/microbiology ; Plasmids ; Plasminogen Activators/genetics/*physiology ; Recombinant Proteins/metabolism ; Spleen/microbiology ; Tissue Plasminogen Activator/metabolism ; Urokinase-Type Plasminogen Activator/metabolism ; Yersinia pestis/*enzymology/isolation & purification/*pathogenicity
    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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    Synaptic amplifier of inflammatory pain in the spinal dorsal horn (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Inflammation and trauma lead to enhanced pain sensitivity (hyperalgesia), which is in part due to altered sensory processing in the spinal cord. The synaptic hypothesis of hyperalgesia, which postulates that hyperalgesia is induced by the activity-dependent long-term potentiation (LTP) in the spinal cord, has been challenged, because in previous studies of pain pathways, LTP was experimentally induced by nerve stimulation at high frequencies ( approximately 100 hertz). This does not, however, resemble the real low-frequency afferent barrage that occurs during inflammation. We identified a synaptic amplifier at the origin of an ascending pain pathway that is switched-on by low-level activity in nociceptive nerve fibers. This model integrates known signal transduction pathways of hyperalgesia without contradiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikeda, Hiroshi -- Stark, Johanna -- Fischer, Harald -- Wagner, Matthias -- Drdla, Ruth -- Jager, Tino -- Sandkuhler, Jurgen -- P 18129/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Hyperalgesia/*physiopathology ; Inflammation/*physiopathology ; Long-Term Potentiation ; Nerve Fibers, Unmyelinated/*physiology ; Neuronal Plasticity ; Nitric Oxide/physiology ; Pain/*physiopathology ; Patch-Clamp Techniques ; Periaqueductal Gray/physiology ; Posterior Horn Cells/*physiopathology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Spinal Cord/physiopathology ; Synapses/physiology ; *Synaptic Transmission
    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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  • 4
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    Animal activism and intimidation of scientists (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stark, Dennis M -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):923-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17106948" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes ; *Animal Experimentation ; *Animal Rights ; Animal Welfare ; Animals ; *Research Personnel ; *Social Behavior ; Terrorism/legislation & jurisprudence ; United States
    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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  • 5
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    STATs find that hanging together can be stimulating (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leung, S -- Li, X -- Stark, G R -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):750-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8701326" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Cytokines/*metabolism ; DNA-Binding Proteins/chemistry/metabolism ; Humans ; Interferon-alpha/metabolism ; Interferon-gamma/metabolism ; Phosphorylation ; Receptor, Interferon alpha-beta ; Receptors, Interferon/metabolism ; STAT1 Transcription Factor ; STAT4 Transcription Factor ; *Signal Transduction ; Trans-Activators/chemistry/*metabolism ; Transcription Factors/metabolism ; *Transcriptional Activation ; src Homology Domains
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  • 6
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    Contribution of STAT SH2 groups to specific interferon signaling by the Jak-STAT pathway (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-03
    Description: In response to specific ligands, various STAT proteins (signal transducers and activators of transcription) are phosphorylated on tyrosine by Jak protein kinases and translocated to the nucleus to direct gene transcription. Selection of a STAT at the interferon gamma receptor as well as specific STAT dimer formation depended on the presence of particular SH2 groups (phosphotyrosine-binding domains), whereas the amino acid sequence surrounding the phosphorylated tyrosine on the STAT could vary. Thus, SH2 groups in STAT proteins may play crucial roles in specificity at the receptor kinase complex and in subsequent dimerization, whereas the kinases are relatively nonspecific.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heim, M H -- Kerr, I M -- Stark, G R -- Darnell, J E Jr -- AI32489/AI/NIAID NIH HHS/ -- AI34420/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 3;267(5202):1347-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7871432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA-Binding Proteins/chemistry/*metabolism ; Interferon-alpha/*pharmacology ; Interferon-gamma/*pharmacology ; Janus Kinase 1 ; Janus Kinase 2 ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Proteins/metabolism ; *Proto-Oncogene Proteins ; Receptors, Interferon/metabolism ; Recombinant Fusion Proteins/metabolism ; STAT1 Transcription Factor ; Signal Transduction ; Trans-Activators/chemistry/*metabolism ; Tyrosine/metabolism
    Print ISSN: 0036-8075
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  • 7
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    Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: Through the study of transcriptional activation in response to interferon alpha (IFN-alpha) and interferon gamma (IFN-gamma), a previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that then phosphorylate substrate proteins called STATs (signal transducers and activators of transcription). The phosphorylated STAT proteins move to the nucleus, bind specific DNA elements, and direct transcription. Recognition of the molecules involved in the IFN-alpha and IFN-gamma pathway has led to discoveries that a number of STAT family members exist and that other polypeptide ligands also use the Jak-STAT molecules in signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darnell, J E Jr -- Kerr, I M -- Stark, G R -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1415-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8197455" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA-Binding Proteins/*metabolism ; Genes ; Genetic Complementation Test ; Humans ; Interferon-Stimulated Gene Factor 3 ; Interferon-Stimulated Gene Factor 3, gamma Subunit ; Interferon-alpha/*pharmacology ; Interferon-gamma/*pharmacology ; Molecular Sequence Data ; Mutation ; Protein-Tyrosine Kinases/metabolism ; Regulatory Sequences, Nucleic Acid ; *Signal Transduction ; Transcription Factors/*metabolism ; *Transcriptional Activation
    Print ISSN: 0036-8075
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  • 8
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    An epigenetic role for maternally inherited piRNAs in transposon silencing (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-29
    Description: In plants and mammals, small RNAs indirectly mediate epigenetic inheritance by specifying cytosine methylation. We found that small RNAs themselves serve as vectors for epigenetic information. Crosses between Drosophila strains that differ in the presence of a particular transposon can produce sterile progeny, a phenomenon called hybrid dysgenesis. This phenotype manifests itself only if the transposon is paternally inherited, suggesting maternal transmission of a factor that maintains fertility. In both P- and I-element-mediated hybrid dysgenesis models, daughters show a markedly different content of Piwi-interacting RNAs (piRNAs) targeting each element, depending on their parents of origin. Such differences persist from fertilization through adulthood. This indicates that maternally deposited piRNAs are important for mounting an effective silencing response and that a lack of maternal piRNA inheritance underlies hybrid dysgenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805124/" 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/PMC2805124/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brennecke, Julius -- Malone, Colin D -- Aravin, Alexei A -- Sachidanandam, Ravi -- Stark, Alexander -- Hannon, Gregory J -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA013106-37/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 28;322(5906):1387-92. doi: 10.1126/science.1165171.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Watson School of Biological Sciences, Howard Hughes Medical Institute, Cold Spring Harbor Laboratory (CSHL), 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19039138" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; Crosses, Genetic ; *DNA Transposable Elements ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/embryology/*genetics/physiology ; *Epigenesis, Genetic ; Female ; Fertility ; Hybridization, Genetic ; Male ; Ovary/metabolism ; Peptide Initiation Factors/genetics/metabolism ; *RNA Interference ; RNA, Small Interfering/*genetics/metabolism
    Print ISSN: 0036-8075
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  • 9
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    The Tasmanian devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-02
    Description: The Tasmanian devil, a marsupial carnivore, is endangered because of the emergence of a transmissible cancer known as devil facial tumor disease (DFTD). This fatal cancer is clonally derived and is an allograft transmitted between devils by biting. We performed a large-scale genetic analysis of DFTD with microsatellite genotyping, a mitochondrial genome analysis, and deep sequencing of the DFTD transcriptome and microRNAs. These studies confirm that DFTD is a monophyletic clonally transmissible tumor and suggest that the disease is of Schwann cell origin. On the basis of these results, we have generated a diagnostic marker for DFTD and identify a suite of genes relevant to DFTD pathology and transmission. We provide a genomic data set for the Tasmanian devil that is applicable to cancer diagnosis, disease evolution, and conservation biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2982769/" 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/PMC2982769/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murchison, Elizabeth P -- Tovar, Cesar -- Hsu, Arthur -- Bender, Hannah S -- Kheradpour, Pouya -- Rebbeck, Clare A -- Obendorf, David -- Conlan, Carly -- Bahlo, Melanie -- Blizzard, Catherine A -- Pyecroft, Stephen -- Kreiss, Alexandre -- Kellis, Manolis -- Stark, Alexander -- Harkins, Timothy T -- Marshall Graves, Jennifer A -- Woods, Gregory M -- Hannon, Gregory J -- Papenfuss, Anthony T -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA013106-38/CA/NCI NIH HHS/ -- R01 GM062534/GM/NIGMS NIH HHS/ -- R01 GM062534-10/GM/NIGMS NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jan 1;327(5961):84-7. doi: 10.1126/science.1180616.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Watson School of Biological Sciences, Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA. elizabeth.murchison@sanger.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044575" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor/analysis ; Bites and Stings/veterinary ; Cell Differentiation ; Facial Neoplasms/diagnosis/genetics/pathology/*veterinary ; *Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, Neoplasm ; Genome, Mitochondrial ; Genotype ; *Marsupialia/genetics ; Membrane Proteins/genetics/metabolism ; MicroRNAs/genetics ; Microsatellite Repeats ; Myelin Basic Protein/genetics ; Nerve Sheath Neoplasms/diagnosis/genetics/pathology/*veterinary ; *Schwann Cells/physiology ; Sequence Analysis, DNA
    Print ISSN: 0036-8075
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  • 10
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    Genome-wide quantitative enhancer activity maps identified by STARR-seq (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-01-19
    Description: Genomic enhancers are important regulators of gene expression, but their identification is a challenge, and methods depend on indirect measures of activity. We developed a method termed STARR-seq to directly and quantitatively assess enhancer activity for millions of candidates from arbitrary sources of DNA, which enables screens across entire genomes. When applied to the Drosophila genome, STARR-seq identifies thousands of cell type-specific enhancers across a broad continuum of strengths, links differential gene expression to differences in enhancer activity, and creates a genome-wide quantitative enhancer map. This map reveals the highly complex regulation of transcription, with several independent enhancers for both developmental regulators and ubiquitously expressed genes. STARR-seq can be used to identify and quantify enhancer activity in other eukaryotes, including humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arnold, Cosmas D -- Gerlach, Daniel -- Stelzer, Christoph -- Boryn, Lukasz M -- Rath, Martina -- Stark, Alexander -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1074-7. doi: 10.1126/science.1232542. Epub 2013 Jan 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology (IMP), Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23328393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping/*methods ; Drosophila melanogaster/genetics/growth & development ; Enhancer Elements, Genetic/*genetics ; Female ; *Gene Expression Regulation ; Gene Expression Regulation, Developmental ; Genome/genetics ; HeLa Cells ; Humans ; Ovary/metabolism ; Sequence Analysis, DNA ; Transcription, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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