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  • 1
    Publication Date: 2011-03-01
    Description: The uptake of dissolved inorganic nitrogen by phytoplankton is an important aspect of the nitrogen cycle of oceans. Here, we present nitrate (NO3-) and ammonium (NH4+) uptake rates in the northeastern Arabian Sea using 15N tracer technique. In this relatively underexplored region, productivity is high during winter due to supply of nutrients by convective mixing caused by the cooling of the surface by the northeast monsoon winds. Studies done during different months (January and late February-early March) of the northeast monsoon 2003 revealed a fivefold increase in the average euphotic zone integrated NO3- uptake from January (2.3 mmolN m−2d−1) to late February-early March (12.7 mmolN m−2d−1). The f-ratio during January appeared to be affected by the winter cooling effect and increased by more than 50% from the southernmost station to the northern open ocean stations, indicating hydrographic and meteorological control. Estimates of NO3- residence time suggested that NO3- entrained in the water column during January contributed to the development of blooms during late February-early March.
    Print ISSN: 1687-9406
    Electronic ISSN: 1687-9414
    Topics: Geosciences
    Published by Hindawi
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  • 2
    Publication Date: 2013-01-22
    Description: The uptake of dissolved inorganic nitrogen by phytoplankton is an important aspect of the nitrogen cycle of oceans. Here, we present nitrate (NO3−) and ammonium (NH4+) uptake rates in the northeastern Arabian Sea using 15N tracer technique. In this relatively underexplored region, productivity is high during winter due to supply of nutrients by convective mixing caused by the cooling of the surface by the northeast monsoon winds. Studies done during different months (January and late February-early March) of the northeast monsoon 2003 revealed a fivefold increase in the average euphotic zone integrated NO3− uptake from January (2.3 mmolN m−2d−1) to late February-early March (12.7 mmolN m−2d−1). The
    Print ISSN: 1687-9406
    Electronic ISSN: 1687-9414
    Topics: Geosciences
    Published by Hindawi
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  • 3
    Electronic Resource
    Electronic Resource
    Weinheim : Wiley-Blackwell
    Zeitschrift für anorganische Chemie 220 (1934), S. 163-168 
    ISSN: 0863-1786
    Keywords: Chemistry ; Inorganic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Weinheim : Wiley-Blackwell
    Zeitschrift für anorganische Chemie 220 (1934), S. 169-171 
    ISSN: 0863-1786
    Keywords: Chemistry ; Inorganic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 5
    Publication Date: 2011-08-18
    Description: Clostridium thermocellum is a thermophilic, obligately anaerobic, Gram-positive bacterium that is a candidate microorganism for converting cellulosic biomass into ethanol through consolidated bioprocessing. Ethanol intolerance is an important metric in terms of process economics, and tolerance has often been described as a complex and likely multigenic trait for which complex gene interactions come into play. Here, we resequence the genome of an ethanol-tolerant mutant, show that the tolerant phenotype is primarily due to a mutated bifunctional acetaldehyde-CoA/alcohol dehydrogenase gene (adhE), hypothesize based on structural analysis that cofactor specificity may be affected, and confirm this hypothesis using enzyme assays. Biochemical assays confirm a complete loss of NADH-dependent activity with concomitant acquisition of NADPH-dependent activity, which likely affects electron flow in the mutant. The simplicity of the genetic basis for the ethanol-tolerant phenotype observed here informs rational engineering of mutant microbial strains for cellulosic ethanol production.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 6
    Publication Date: 2009-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raman, Malavika -- Harper, J Wade -- R01 AG011085/AG/NIA NIH HHS/ -- R01 GM070565/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Dec 3;462(7273):585-6. doi: 10.1038/462585a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19956252" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Biology ; Cyclin E/metabolism ; Humans ; Models, Molecular ; Proteasome Endopeptidase Complex/*physiology ; Ubiquitin-Activating Enzymes/metabolism ; Ubiquitination/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2013-03-19
    Description: The PARKIN ubiquitin ligase (also known as PARK2) and its regulatory kinase PINK1 (also known as PARK6), often mutated in familial early-onset Parkinson's disease, have central roles in mitochondrial homeostasis and mitophagy. Whereas PARKIN is recruited to the mitochondrial outer membrane (MOM) upon depolarization via PINK1 action and can ubiquitylate porin, mitofusin and Miro proteins on the MOM, the full repertoire of PARKIN substrates--the PARKIN-dependent ubiquitylome--remains poorly defined. Here we use quantitative diGly capture proteomics (diGly) to elucidate the ubiquitylation site specificity and topology of PARKIN-dependent target modification in response to mitochondrial depolarization. Hundreds of dynamically regulated ubiquitylation sites in dozens of proteins were identified, with strong enrichment for MOM proteins, indicating that PARKIN dramatically alters the ubiquitylation status of the mitochondrial proteome. Using complementary interaction proteomics, we found depolarization-dependent PARKIN association with numerous MOM targets, autophagy receptors, and the proteasome. Mutation of the PARKIN active site residue C431, which has been found mutated in Parkinson's disease patients, largely disrupts these associations. Structural and topological analysis revealed extensive conservation of PARKIN-dependent ubiquitylation sites on cytoplasmic domains in vertebrate and Drosophila melanogaster MOM proteins. These studies provide a resource for understanding how the PINK1-PARKIN pathway re-sculpts the proteome to support mitochondrial homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3641819/" 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/PMC3641819/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sarraf, Shireen A -- Raman, Malavika -- Guarani-Pereira, Virginia -- Sowa, Mathew E -- Huttlin, Edward L -- Gygi, Steven P -- Harper, J Wade -- CA139885/CA/NCI NIH HHS/ -- GM067945/GM/NIGMS NIH HHS/ -- GM070565/GM/NIGMS NIH HHS/ -- GM095567/GM/NIGMS NIH HHS/ -- R01 GM067945/GM/NIGMS NIH HHS/ -- R01 GM070565/GM/NIGMS NIH HHS/ -- R01 GM095567/GM/NIGMS NIH HHS/ -- England -- Nature. 2013 Apr 18;496(7445):372-6. doi: 10.1038/nature12043. Epub 2013 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23503661" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Drosophila Proteins/metabolism ; Drosophila melanogaster/metabolism ; Humans ; *Membrane Potential, Mitochondrial ; Mice ; Mitochondria/chemistry/*metabolism ; Mitochondrial Membranes/*metabolism ; Mitochondrial Proteins/*metabolism ; Protein Kinases/metabolism ; Proteome/*metabolism ; Proteomics ; Ubiquitin-Protein Ligases/*metabolism ; *Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2011-12-27
    Description: An unusual feature of the cerebellar cortex is that its output neurons, Purkinje cells, release GABA (gamma-aminobutyric acid). Their high intrinsic firing rates (50 Hz) and extensive convergence predict that their target neurons in the cerebellar nuclei would be largely inhibited unless Purkinje cells pause their spiking, yet Purkinje and nuclear neuron firing rates do not always vary inversely. One indication of how these synapses transmit information is that populations of Purkinje neurons synchronize their spikes during cerebellar behaviours. If nuclear neurons respond to Purkinje synchrony, they may encode signals from subsets of inhibitory inputs. Here we show in weanling and adult mice that nuclear neurons transmit the timing of synchronous Purkinje afferent spikes, owing to modest Purkinje-to-nuclear convergence ratios ( approximately 40:1), fast inhibitory postsynaptic current kinetics (tau(decay) = 2.5 ms) and high intrinsic firing rates ( approximately 90 Hz). In vitro, dynamically clamped asynchronous inhibitory postsynaptic potentials mimicking Purkinje afferents suppress nuclear cell spiking, whereas synchronous inhibitory postsynaptic potentials entrain nuclear cell spiking. With partial synchrony, nuclear neurons time-lock their spikes to the synchronous subpopulation of inputs, even when only 2 out of 40 afferents synchronize. In vivo, nuclear neurons reliably phase-lock to regular trains of molecular layer stimulation. Thus, cerebellar nuclear neurons can preferentially relay the spike timing of synchronized Purkinje cells to downstream premotor areas.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3268051/" 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/PMC3268051/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Person, Abigail L -- Raman, Indira M -- F32 NS067831/NS/NINDS NIH HHS/ -- F32 NS067831-02/NS/NINDS NIH HHS/ -- F32-NS067831/NS/NINDS NIH HHS/ -- R01 NS039395/NS/NINDS NIH HHS/ -- R01 NS039395-13/NS/NINDS NIH HHS/ -- R01-NS39395/NS/NINDS NIH HHS/ -- England -- Nature. 2011 Dec 25;481(7382):502-5. doi: 10.1038/nature10732.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Northwestern University, Evanston, Illinois 60208, USA. a-person@northwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22198670" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Animals ; Cerebellar Cortex/cytology ; Cerebellar Nuclei/*physiology ; Inhibitory Postsynaptic Potentials/*physiology ; Kinetics ; Mice ; Mice, Inbred C57BL ; Purkinje Cells/*physiology ; Time Factors ; Weaning
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2013-03-13
    Description: The calcium-activated chloride channel anoctamin 1 (ANO1) is located within the 11q13 amplicon, one of the most frequently amplified chromosomal regions in human cancer, but its functional role in tumorigenesis has remained unclear. The 11q13 region is amplified in ∼15% of breast cancers. Whether ANO1 is amplified in breast tumors,...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 10
    Publication Date: 2014-07-09
    Description: Nephronophthisis (NPHP) is the major cause of pediatric renal failure, yet the disease remains poorly understood, partly due to the lack of appropriate animal models. Joubert syndrome (JBTS) is an inherited ciliopathy giving rise to NPHP with cerebellar vermis aplasia and retinal degeneration. Among patients with JBTS and a cerebello-oculo-renal...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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