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111.
Bighead and silver carp are well established in the Mississippi River basin following their accidental introduction in the
1980s. Referred to collectively as Asian carp, these species are filter feeders consuming phytoplankton and zooplankton. We
examined diet overlap and electivity of Asian carp and three native filter feeding fishes, bigmouth buffalo, gizzard shad,
and paddlefish, in backwater lakes of the Illinois and Mississippi rivers. Rotifers, Keratella spp., Brachionus spp., and Trichocerca spp., were the most common prey items consumed by Asian carp and gizzard shad, whereas crustacean zooplankton were the preferred
prey of paddlefish. Bigmouth buffalo diet was broad, including both rotifers and crustacean zooplankton. Dietary overlap with
Asian carp was greatest for gizzard shad followed by bigmouth buffalo, but we found little diet overlap for paddlefish. Diet
similarity based on taxonomy correlated strongly with diet similarity based on size suggesting filtration efficiency influenced
the overlap patterns we observed. Although rotifers were the most common prey item consumed by both bighead and silver carp,
we found a negative relation between silver carp CPUE and cladoceran density. The competitive effect of Asian carp on native
fishes may be forestalled because of the high productivity of Illinois and Mississippi river habitats, yet the potential for
negative consequences of Asian carp in less productive ecosystems, including Lake Michigan, should not be underestimated. 相似文献
112.
Herpes simplex virus type-1 origin-binding protein (UL9 protein) initiates viral replication by unwinding the origins. It possesses sequence-specific DNA-binding activity, single-stranded DNA-binding activity, DNA helicase activity, and ATPase activity that is strongly stimulated by single-stranded DNA. We have examined the role of cysteines in its action as a DNA helicase. The DNA helicase and DNA-dependent ATPase activities of UL9 protein were stimulated by reducing agent and specifically inactivated by the sulfhydryl-specific reagent N-ethylmaleimide. To identify the cysteine responsible for this phenomenon, a conserved cysteine in the vicinity of the ATP-binding site (cysteine 111) was mutagenized to alanine. UL9C111A protein exhibits defects in its DNA helicase and DNA-dependent ATPase activities and was unable to support origin-specific DNA replication in vivo. A kinetic analysis indicates that these defects are due to the inability of single-stranded DNA to induce high affinity ATP binding in UL9C111A protein. The DNA-dependent ATPase activity of UL9C111A protein is resistant to N-ethylmaleimide, while its DNA helicase activity remains sensitive. Accordingly, sensitivity of UL9 protein to N-ethylmaleimide is due to at least two cysteines. Cysteine 111 is involved in coupling single-stranded DNA binding to ATP-binding and subsequent hydrolysis, while a second cysteine is involved in coupling ATP hydrolysis to DNA unwinding. 相似文献
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S. R. Sampson E. Bucris M. Horovitz-Fried A. Parnas S. Kahana G. Abitbol M. Chetboun T. Rosenzweig C. Brodie S. Frankel 《Apoptosis : an international journal on programmed cell death》2010,15(10):1165-1176
Insulin resistance results, in part, from impaired insulin signaling in insulin target tissues. Consequently, increased levels
of insulin are necessary to control plasma glucose levels. The effects of elevated insulin levels on pancreatic beta (β) cell
function, however, are unclear. In this study, we investigated the possibility that insulin may influence survival of pancreatic
β cells. Studies were conducted on RINm, RINm5F and Min-6 pancreatic β-cells. Cell death was induced by treatment with H2O2, and was estimated by measurements of LDH levels, viability assay (Cell-Titer Blue), propidium iodide staining and FACS analysis,
and mitochondrial membrane potential (JC-1). In addition, levels of cleaved caspase-3 and caspase activity were determined.
Treatment with H2O2 increased cell death; this effect was increased by simultaneous treatment of cells with insulin. Insulin treatment alone
caused a slight increase in cell death. Inhibition of caspase-3 reduced the effect of insulin to increase H2O2-induced cell death. Insulin increased ROS production by pancreatic β cells and increased the effect of H2O2. These effects were increased by inhibition of IR signaling, indicative of an effect independent of the IR cascade. We conclude
that elevated levels of insulin may act to exacerbate cell death induced by H2O2 and, perhaps, other inducers of apoptosis. 相似文献
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A.H.M.Mahbubul Huq Rhonda S. Lovell Margaret J. Sampson William K. Decker Mary Beth Dinulos Christine M. Disteche William J. Craigen 《Genomics》1996,36(3):530
Glycerol kinase (Gyk) participates in the metabolism of endogenously derived and dietary glycerol. Deficiency of the human enzyme activity is an X-linked recessive disorder with a clinical picture varying from childhood metabolic crisis to asymptomatic adults incidentally identified by hyperlipidemia screening (pseudohypertriglyceridemia). Gyk is a member of a small group of kinases termed ambiquitous enzymes that are found in the cytosol or as membrane-bound enzymes associated with the voltage-dependent anion channel of the mitochondrial outer membrane. It was recently reported that in humans there are X-linked and autosomal copies of Gyk sequences, both apparently functional genes and processed pseudogenes. To understand the role of Gyk in normal metabolism and the variable clinical features seen with Gyk deficiency, we have characterized the mouse Gyk gene. We present the sequence of a full-length mouse Gyk cDNA that is alternatively spliced in brain. The Gyk gene was mapped to the mouse X chromosome by both fluorescencein situhybridization and an interspecies backcross panel, demonstrating conservation of synteny withdmd.To confirm the functional identity of the cDNA, transient transfection of the cDNA into COS7 cells was shown to cause a marked elevation in glycerol kinase activity. 相似文献
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James A. Gregory Ariel Shepley‐McTaggart Michelle Umpierrez Barry K. Hurlburt Soheila J. Maleki Hugh A. Sampson Stephen P. Mayfield M. Cecilia Berin 《Plant biotechnology journal》2016,14(7):1541-1550
Peanut allergy is an IgE‐mediated adverse reaction to a subset of proteins found in peanuts. Immunotherapy aims to desensitize allergic patients through repeated and escalating exposures for several months to years using extracts or flours. The complex mix of proteins and variability between preparations complicates immunotherapy studies. Moreover, peanut immunotherapy is associated with frequent negative side effects and patients are often at risk of allergic reactions once immunotherapy is discontinued. Allergen‐specific approaches using recombinant proteins are an attractive alternative because they allow more precise dosing and the opportunity to engineer proteins with improved safety profiles. We tested whether Ara h 1 and Ara h 2, two major peanut allergens, could be produced using chloroplast of the unicellular eukaryotic alga, Chlamydomonas reinhardtii. C. reinhardtii is novel host for producing allergens that is genetically tractable, inexpensive and easy to grow, and is able to produce more complex proteins than bacterial hosts. Compared to the native proteins, algal‐produced Ara h 1 core domain and Ara h 2 have a reduced affinity for IgE from peanut‐allergic patients. We further found that immunotherapy using algal‐produced Ara h 1 core domain confers protection from peanut‐induced anaphylaxis in a murine model of peanut allergy. 相似文献
120.
Xiaohong R. Yang Melissa Rotunno Yanzi Xiao Christian Ingvar Hildur Helgadottir Lorenza Pastorino Remco van Doorn Hunter Bennett Cole Graham Joshua N. Sampson Michael Malasky Aurelie Vogt Bin Zhu Giovanna Bianchi-Scarra William Bruno Paola Queirolo Giuseppe Fornarini Johan Hansson Rainer Tuominen Laurie Burdett Belynda Hicks Amy Hutchinson Kristine Jones Meredith Yeager Stephen J. Chanock Maria Teresa Landi Veronica Höiom Håkan Olsson Nelleke Gruis Paola Ghiorzo Margaret A. Tucker Alisa M. Goldstein 《Human genetics》2016,135(11):1241-1249