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  • Mice  (3)
  • *Caenorhabditis elegans/enzymology/genetics/microbiology  (1)
  • 1
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    Natural polymorphisms in C. elegans HECW-1 E3 ligase affect pathogen avoidance behaviour (2011)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2011-11-18
    Beschreibung: Heritable variation in behavioural traits generally has a complex genetic basis, and thus naturally occurring polymorphisms that influence behaviour have been defined only in rare instances. The isolation of wild strains of Caenorhabditis elegans has facilitated the study of natural genetic variation in this species and provided insights into its diverse microbial ecology. C. elegans responds to bacterial infection with conserved innate immune responses and, although lacking the immunological memory of vertebrate adaptive immunity, shows an aversive learning response to pathogenic bacteria. Here, we report the molecular characterization of naturally occurring coding polymorphisms in a C. elegans gene encoding a conserved HECT domain-containing E3 ubiquitin ligase, HECW-1. We show that two distinct polymorphisms in neighbouring residues of HECW-1 each affect C. elegans behavioural avoidance of a lawn of Pseudomonas aeruginosa. Neuron-specific rescue and ablation experiments and genetic interaction analysis indicate that HECW-1 functions in a pair of sensory neurons to inhibit P. aeruginosa lawn avoidance behaviour through inhibition of the neuropeptide receptor NPR-1 (ref. 10), which we have previously shown promotes P. aeruginosa lawn avoidance behaviour. Our data establish a molecular basis for natural variation in a C. elegans behaviour that may undergo adaptive changes in response to microbial pathogens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3245782/" 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/PMC3245782/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Howard C -- Paek, Jennifer -- Kim, Dennis H -- GM084477/GM/NIGMS NIH HHS/ -- R01 GM084477/GM/NIGMS NIH HHS/ -- R01 GM084477-05/GM/NIGMS NIH HHS/ -- England -- Nature. 2011 Nov 16;480(7378):525-9. doi: 10.1038/nature10643.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22089131" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Behavior, Animal ; *Caenorhabditis elegans/enzymology/genetics/microbiology ; Caenorhabditis elegans Proteins/*genetics/*metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Enzymologic ; *Polymorphism, Genetic ; Pseudomonas aeruginosa/*physiology ; Receptors, Neuropeptide Y/metabolism ; Sensory Receptor Cells/enzymology ; Ubiquitin-Protein Ligases/*genetics/*metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Two replication fork maintenance pathways fuse inverted repeats to rearrange chromosomes (2013)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2013-09-10
    Beschreibung: Replication fork maintenance pathways preserve chromosomes, but their faulty application at nonallelic repeats could generate rearrangements causing cancer, genomic disorders and speciation. Potential causal mechanisms are homologous recombination and error-free postreplication repair (EF-PRR). Homologous recombination repairs damage-induced DNA double-strand breaks (DSBs) and single-ended DSBs within replication. To facilitate homologous recombination, the recombinase RAD51 and mediator BRCA2 form a filament on the 3' DNA strand at a break to enable annealing to the complementary sister chromatid while the RecQ helicase, BLM (Bloom syndrome mutated) suppresses crossing over to prevent recombination. Homologous recombination also stabilizes and restarts replication forks without a DSB. EF-PRR bypasses DNA incongruities that impede replication by ubiquitinating PCNA (proliferating cell nuclear antigen) using the RAD6-RAD18 and UBC13-MMS2-RAD5 ubiquitin ligase complexes. Some components are common to both homologous recombination and EF-PRR such as RAD51 and RAD18. Here we delineate two pathways that spontaneously fuse inverted repeats to generate unstable chromosomal rearrangements in wild-type mouse embryonic stem (ES) cells. Gamma-radiation induced a BLM-regulated pathway that selectively fused identical, but not mismatched, repeats. By contrast, ultraviolet light induced a RAD18-dependent pathway that efficiently fused mismatched repeats. Furthermore, TREX2 (a 3'--〉5' exonuclease) suppressed identical repeat fusion but enhanced mismatched repeat fusion, clearly separating these pathways. TREX2 associated with UBC13 and enhanced PCNA ubiquitination in response to ultraviolet light, consistent with it being a novel member of EF-PRR. RAD18 and TREX2 also suppressed replication fork stalling in response to nucleotide depletion. Interestingly, replication fork stalling induced fusion for identical and mismatched repeats, implicating faulty replication as a causal mechanism for both pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3805358/" 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/PMC3805358/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Lingchuan -- Kim, Tae Moon -- Son, Mi Young -- Kim, Sung-A -- Holland, Cory L -- Tateishi, Satoshi -- Kim, Dong Hyun -- Yew, P Renee -- Montagna, Cristina -- Dumitrache, Lavinia C -- Hasty, Paul -- 1 R01 CA123203-01A1/CA/NCI NIH HHS/ -- 2P01AG017242-12/AG/NIA NIH HHS/ -- P30 CA054174/CA/NCI NIH HHS/ -- P30CA013330/CA/NCI NIH HHS/ -- R01 CA123203/CA/NCI NIH HHS/ -- England -- Nature. 2013 Sep 26;501(7468):569-72. doi: 10.1038/nature12500. Epub 2013 Sep 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Medicine/Institute of Biotechnology, The Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78245-3207, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24013173" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Base Sequence ; Chromosomal Instability/*genetics ; Chromosome Breakage ; Chromosomes, Mammalian/*genetics ; DNA Breaks, Double-Stranded ; DNA Repair/*genetics ; DNA Replication/*genetics ; DNA-Binding Proteins/metabolism ; Embryonic Stem Cells/metabolism ; Exodeoxyribonucleases/metabolism ; Homologous Recombination/*genetics ; Hydroxyurea/pharmacology ; Inverted Repeat Sequences/*genetics ; Mice ; Nucleotides/deficiency/metabolism ; Proliferating Cell Nuclear Antigen/metabolism ; Rad51 Recombinase/metabolism ; RecQ Helicases/metabolism ; Ubiquitin-Conjugating Enzymes/metabolism ; Ubiquitination/radiation effects ; Ultraviolet Rays
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Reversing EphB2 depletion rescues cognitive functions in Alzheimer model (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-11-30
    Beschreibung: Amyloid-beta oligomers may cause cognitive deficits in Alzheimer's disease by impairing neuronal NMDA-type glutamate receptors, whose function is regulated by the receptor tyrosine kinase EphB2. Here we show that amyloid-beta oligomers bind to the fibronectin repeats domain of EphB2 and trigger EphB2 degradation in the proteasome. To determine the pathogenic importance of EphB2 depletions in Alzheimer's disease and related models, we used lentiviral constructs to reduce or increase neuronal expression of EphB2 in memory centres of the mouse brain. In nontransgenic mice, knockdown of EphB2 mediated by short hairpin RNA reduced NMDA receptor currents and impaired long-term potentiation in the dentate gyrus, which are important for memory formation. Increasing EphB2 expression in the dentate gyrus of human amyloid precursor protein transgenic mice reversed deficits in NMDA receptor-dependent long-term potentiation and memory impairments. Thus, depletion of EphB2 is critical in amyloid-beta-induced neuronal dysfunction. Increasing EphB2 levels or function could be beneficial in Alzheimer's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030448/" 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/PMC3030448/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cisse, Moustapha -- Halabisky, Brian -- Harris, Julie -- Devidze, Nino -- Dubal, Dena B -- Sun, Binggui -- Orr, Anna -- Lotz, Gregor -- Kim, Daniel H -- Hamto, Patricia -- Ho, Kaitlyn -- Yu, Gui-Qiu -- Mucke, Lennart -- AG011385/AG/NIA NIH HHS/ -- AG022074/AG/NIA NIH HHS/ -- K08 AG034531/AG/NIA NIH HHS/ -- NS041787/NS/NINDS NIH HHS/ -- P01 AG022074/AG/NIA NIH HHS/ -- P01 AG022074-09/AG/NIA NIH HHS/ -- R01 AG011385/AG/NIA NIH HHS/ -- R01 AG011385-08/AG/NIA NIH HHS/ -- R01 NS041787/NS/NINDS NIH HHS/ -- R01 NS041787-09/NS/NINDS NIH HHS/ -- RR18928-01/RR/NCRR NIH HHS/ -- England -- Nature. 2011 Jan 6;469(7328):47-52. doi: 10.1038/nature09635. Epub 2010 Nov 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21113149" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alzheimer Disease/*physiopathology/*therapy ; Amyloid beta-Peptides/metabolism ; Animals ; Cell Line ; Cells, Cultured ; Cognition/*physiology ; Dentate Gyrus/metabolism ; Disease Models, Animal ; Humans ; Long-Term Potentiation ; Memory/physiology ; Mice ; Mice, Transgenic ; Neuronal Plasticity ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Rats ; Receptor, EphB2/chemistry/*deficiency/genetics/*metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    A physically transient form of silicon electronics (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2012-09-29
    Beschreibung: A remarkable feature of modern silicon electronics is its ability to remain physically invariant, almost indefinitely for practical purposes. Although this characteristic is a hallmark of applications of integrated circuits that exist today, there might be opportunities for systems that offer the opposite behavior, such as implantable devices that function for medically useful time frames but then completely disappear via resorption by the body. We report a set of materials, manufacturing schemes, device components, and theoretical design tools for a silicon-based complementary metal oxide semiconductor (CMOS) technology that has this type of transient behavior, together with integrated sensors, actuators, power supply systems, and wireless control strategies. An implantable transient device that acts as a programmable nonantibiotic bacteriocide provides a system-level example.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3786576/" 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/PMC3786576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, Suk-Won -- Tao, Hu -- Kim, Dae-Hyeong -- Cheng, Huanyu -- Song, Jun-Kyul -- Rill, Elliott -- Brenckle, Mark A -- Panilaitis, Bruce -- Won, Sang Min -- Kim, Yun-Soung -- Song, Young Min -- Yu, Ki Jun -- Ameen, Abid -- Li, Rui -- Su, Yewang -- Yang, Miaomiao -- Kaplan, David L -- Zakin, Mitchell R -- Slepian, Marvin J -- Huang, Yonggang -- Omenetto, Fiorenzo G -- Rogers, John A -- EB002520/EB/NIBIB NIH HHS/ -- P41 EB002520/EB/NIBIB NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1640-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials Science and Engineering, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019646" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Absorbable Implants ; Animals ; Anti-Bacterial Agents ; Electric Power Supplies ; *Electronics ; Metals ; Mice ; Mice, Inbred BALB C ; Oxides ; *Semiconductors ; *Silicon ; Transistors, Electronic ; Wireless Technology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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