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  • 1
    Electronic Resource
    Electronic Resource
    Discovery of a new photoinduced electron trap state shallower than the DX center in Si doped AlxGa1−xAs (1989)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 66 (1989), S. 5632-5634 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: We have found a new electron trap state in Si-doped AlxGa1−xAs by deep level transient spectroscopy and constant temperature capacitance transient measurements under strong light illumination. This new trap is shallower than the DX center associated with Si impurity in that its emission and capture activation energies are equal to 0.20±0.05 and 0.17±0.05 eV, respectively. Its maximum concentration is comparable to the concentration of the DX center. Possible origins of this new trap and its relationship to the DX center are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.343672
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Charge recombination between the oxidized high-potential c-type cytochromes and Q^-"A in reaction centers from Rhodopseudomonas viridis
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Bioenergetics 1015 (1990), S. 96-108 
    Details
    ISSN: 0005-2728
    Keywords: (Rps. viridis) ; Charge recombination ; Cytochrome ; Electron transfer ; Photosynthesis ; Reaction center
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0005-2728(90)90220-X
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  • 3
    Electronic Resource
    Electronic Resource
    Sulfhydryl modifying reagents inhibit Q A − oxidation in reaction centers from Rhodobacter sphaeroides and Capsulatus, but not Rhodopseudomonas viridis (1990)
    Springer
    Photosynthesis research 26 (1990), S. 171-179 
    Details
    ISSN: 1573-5079
    Keywords: Photosynthesis ; reaction centers ; quinones ; sulfhydryl reagents ; Rb. sphaeroides ; Rb. capsulatus ; Rp. viridis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The effects of various sulfhydryl-modifying reagents on reaction centers (RCs) from purple photosynthetic bacteria have been examined, with particular emphasis on the activity of the acceptor quinones, QA and QB, comprising the two electron gate. Mercurial reagents, especially p-chloromercuribenzenesulfonate (pCMBS), were effective in inhibiting QB function in RCs from Rhodobacter sphaeroides and Rb. capsulatus, but not in Rhodopseudomonas viridis. The inhibition was fully reversible by dialysis against dithiothreitol (DTT). The effect on QB function was not an apparent one mediated by an alteration in the redox potential of QA. N-ethylmaleimide (NEM) had no effect on any of the quinone functions, even at very high concentrations. Comparison of the X-ray structures of the RCs from Rb. sphaeroides and Rp. viridis and the known amino acid sequences for all three bacterial RCs suggest that a cysteine residue at position 108 in the L subunit of the Rhodobacter species is the most likely candidate for the site of action of the mercurial reagents. This was strongly supported by the absence of any effect of pCMBS on a site specific mutation of Rb. sphaeroides (L108CS) with residue L108 changed from cysteine to serine. These results imply a long distance (〉20 Å) effect on the functioning of QB, perhaps involving a relatively gross structural alteration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00033130
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  • 4
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    Mitochondrial Fission of Smooth Muscle Cells Is Involved in Artery Constriction [Vessels] (2016)
    American Heart Association (AHA)
    Details
    Publication Date: 2016-10-13
    Description: Mitochondria are dynamic organelles and continuously undergo fission and fusion processes. Mitochondrial fission is involved in multiple physiological or pathological processes, but the role of mitochondrial fission of smooth muscle cells in artery constriction is unknown. The role of mitochondrial fission of smooth muscle cells in arterial function was investigated by measuring the tension of rat mesenteric arteries and thoracic aorta and by evaluating mitochondrial fission, mitochondrial reactive oxygen species, and cytosolic [Ca 2+ ] i in rat vascular smooth muscle cells. Mitochondrial fission inhibitors mdivi-1 and dynasore antagonized phenylephrine- and high K + –induced constriction of rat mesenteric arteries. Mdivi-1 relaxed phenylephrine-induced constriction, and mdivi-1 pretreatment prevented phenylephrine-induced constriction in mice, rat aorta, and human mesenteric arteries. Phenylephrine- and high K + –induced increase of mitochondrial fission in smooth muscle cells of rat aorta and the increase was inhibited by mdivi-1. Mdivi-1 inhibited high K + –induced increases of mitochondrial fission, mitochondrial reactive oxygen species, and cytosolic [Ca 2+ ] i in rat vascular smooth muscle cells. Prechelation of cytosolic Ca 2+ prevented high K + –induced cytosolic [Ca 2+ ] i increase, mitochondrial fission, and mitochondrial reactive oxygen species overproduction. Mitochondria-targeted antioxidant mito-TEMPO antagonized phenylephrine- and high K + –induced constriction of rat mesenteric arteries. Nitroglycerin and ROCK (Rho-associated protein kinase) inhibitor Y27632, the 2 vasodilators with different vasorelaxant mechanisms, relaxed high K + –induced vasoconstriction and inhibited high K + –induced mitochondrial fission. In conclusion, the mitochondrial fission of smooth muscle cells is involved in artery constriction.
    Keywords: Basic Science Research, Contractile Function, Vascular Biology, Hypertension, Pharmacology
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 5
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    Heme-binding Dps of P. gingivalis [Protein Structure and Folding] (2012)
    The American Society for Biochemistry and Molecular Biology (ASBMB)
    Details
    Publication Date: 2012-12-08
    Description: The widely expressed DNA-protective protein from starved-cells (Dps) family proteins are considered major contributors to prokaryotic resistance to stress. We show here that Porphyromonas gingivalis Dps (PgDps), previously described as an iron-storage and DNA-binding protein, also mediates heme sequestration. We determined that heme binds strongly to PgDps with an apparent Kd of 3.7 × 10−8 m and is coordinated by a single surface-located cysteine at the fifth axial ligand position. Heme and iron sequestered in separate sites by PgDps provide protection of DNA from H2O2-mediated free radical damage and were found to be important for growth of P. gingivalis under excess heme as the only iron source. Conservation of the heme-coordinating cysteine among Dps isoforms from the Bacteroidales order suggests that this function may be a common feature within these anaerobic bacteria.
    Print ISSN: 0021-9258
    Electronic ISSN: 1083-351X
    Topics: Biology , Chemistry and Pharmacology
    Published by The American Society for Biochemistry and Molecular Biology (ASBMB)
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  • 6
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    FPR1 on Lens Epithelial Cells [Immunology] (2012)
    The American Society for Biochemistry and Molecular Biology (ASBMB)
    Details
    Publication Date: 2012-11-24
    Description: Formyl peptide receptor 1 (FPR1) is a G protein-coupled chemoattractant receptor expressed mainly on leukocytes. Surprisingly, aging Fpr1−/− mice develop spontaneous lens degeneration without inflammation or infection (J.-L. Gao et al., manuscript in preparation). Therefore, we hypothesized that FPR1 is functionally expressed directly on lens epithelial cells, the only cell type in the lens. Consistent with this, the human fetal lens epithelial cell line FHL 124 expressed FPR1 mRNA and was strongly FPR1 protein-positive by Western blot and FACS. Competition binding using FPR1 ligands N-formyl-Nle-Leu-Phe-Nle-Tyr-Lys (Nle = Norleucine), formylmethionylleucylphenylalanine, and peptide W revealed the same profile for FHL 124 cells, neutrophils, and FPR1-transfected HEK 293 cells. Saturation binding with fluorescein-labeled N-formyl-Nle-Leu-Phe-Nle-Tyr-Lys revealed ∼2500 specific binding sites on FHL-124 cells (KD ∼ 0.5 nm) versus ∼40,000 sites on neutrophils (KD = 3.2 nm). Moreover, formylmethionylleucylphenylalanine induced pertussis toxin-sensitive Ca2+ flux in FHL 124 cells, consistent with classic Gi-mediated FPR1 signaling. FHL 124 cell FPR1 was atypical in that it resisted agonist-induced internalization. Expression of FPR1 was additionally supported by detection of the intact full-length open reading frame in sequenced cDNA from FHL 124 cells. Thus, FHL-124 cells express functional FPR1, which is consistent with a direct functional role for FPR1 in the lens, as suggested by the phenotype of Fpr1 knock-out mice.
    Print ISSN: 0021-9258
    Electronic ISSN: 1083-351X
    Topics: Biology , Chemistry and Pharmacology
    Published by The American Society for Biochemistry and Molecular Biology (ASBMB)
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  • 7
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    The Loss of RGS Protein-G{alpha}i2 Interactions Results in Markedly Impaired Mouse Neutrophil Trafficking to Inflammatory Sites [Articles] (2012)
    The American Society for Microbiology (ASM)
    Details
    Publication Date: 2012-10-26
    Description: Neutrophils are first responders rapidly mobilized to inflammatory sites by a tightly regulated, nonredundant hierarchy of chemoattractants. These chemoattractants engage neutrophil cell surface receptors triggering heterotrimeric G-protein Gα i subunits to exchange GDP for GTP. By limiting the duration that Gα i subunits remain GTP bound, RGS proteins modulate chemoattractant receptor signaling. Here, we show that neutrophils with a genomic knock in of a mutation that disables r egulator of G -protein s ignaling (RGS)-Gα i2 interactions accumulate in the bone marrow and mobilize poorly to inflammatory sites. These defects are attributable to enhanced sensitivity to background signals, prolonged chemoattractant receptor signaling, and inappropriate CXCR2 downregulation. Intravital imaging revealed a failure of the mutant neutrophils to accumulate at and stabilize sites of sterile inflammation. Furthermore, these mice could not control a nonlethal Staphylococcus aureus infection. Neutrophil RGS proteins establish a threshold for Gα i activation, helping to coordinate desensitization mechanisms. Their loss renders neutrophils functionally incompetent.
    Print ISSN: 0270-7306
    Electronic ISSN: 1098-5549
    Topics: Biology , Medicine
    Published by The American Society for Microbiology (ASM)
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  • 8
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    A conserved intronic U1 snRNP-binding sequence promotes trans-splicing in Drosophila [Research Papers] (2015)
    Cold Spring Harbor Laboratory Press
    Details
    Publication Date: 2015-04-03
    Description: Unlike typical cis -splicing, trans -splicing joins exons from two separate transcripts to produce chimeric mRNA and has been detected in most eukaryotes. Trans -splicing in trypanosomes and nematodes has been characterized as a spliced leader RNA-facilitated reaction; in contrast, its mechanism in higher eukaryotes remains unclear. Here we investigate mod(mdg4) , a classic trans -spliced gene in Drosophila , and report that two critical RNA sequences in the middle of the last 5' intron, TSA and TSB, promote trans -splicing of mod(mdg4) . In TSA, a 13-nucleotide (nt) core motif is conserved across Drosophila species and is essential and sufficient for trans -splicing, which binds U1 small nuclear RNP (snRNP) through strong base-pairing with U1 snRNA. In TSB, a conserved secondary structure acts as an enhancer. Deletions of TSA and TSB using the CRISPR/Cas9 system result in developmental defects in flies. Although it is not clear how the 5' intron finds the 3' introns, compensatory changes in U1 snRNA rescue trans -splicing of TSA mutants, demonstrating that U1 recruitment is critical to promote trans -splicing in vivo. Furthermore, TSA core-like motifs are found in many other trans -spliced Drosophila genes, including lola. These findings represent a novel mechanism of trans -splicing, in which RNA motifs in the 5' intron are sufficient to bring separate transcripts into close proximity to promote trans -splicing.
    Print ISSN: 0890-9369
    Topics: Biology
    Published by Cold Spring Harbor Laboratory Press
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  • 9
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    Mitochondrial Fission of Smooth Muscle Cells Is Involved in Artery ConstrictionNovelty and Significance [Vessels] (2016)
    American Heart Association (AHA)
    Details
    Publication Date: 2016-11-05
    Description: Mitochondria are dynamic organelles and continuously undergo fission and fusion processes. Mitochondrial fission is involved in multiple physiological or pathological processes, but the role of mitochondrial fission of smooth muscle cells in artery constriction is unknown. The role of mitochondrial fission of smooth muscle cells in arterial function was investigated by measuring the tension of rat mesenteric arteries and thoracic aorta and by evaluating mitochondrial fission, mitochondrial reactive oxygen species, and cytosolic [Ca2+]i in rat vascular smooth muscle cells. Mitochondrial fission inhibitors mdivi-1 and dynasore antagonized phenylephrine- and high K+–induced constriction of rat mesenteric arteries. Mdivi-1 relaxed phenylephrine-induced constriction, and mdivi-1 pretreatment prevented phenylephrine-induced constriction in mice, rat aorta, and human mesenteric arteries. Phenylephrine- and high K+–induced increase of mitochondrial fission in smooth muscle cells of rat aorta and the increase was inhibited by mdivi-1. Mdivi-1 inhibited high K+–induced increases of mitochondrial fission, mitochondrial reactive oxygen species, and cytosolic [Ca2+]i in rat vascular smooth muscle cells. Prechelation of cytosolic Ca2+ prevented high K+–induced cytosolic [Ca2+]i increase, mitochondrial fission, and mitochondrial reactive oxygen species overproduction. Mitochondria-targeted antioxidant mito-TEMPO antagonized phenylephrine- and high K+–induced constriction of rat mesenteric arteries. Nitroglycerin and ROCK (Rho-associated protein kinase) inhibitor Y27632, the 2 vasodilators with different vasorelaxant mechanisms, relaxed high K+–induced vasoconstriction and inhibited high K+–induced mitochondrial fission. In conclusion, the mitochondrial fission of smooth muscle cells is involved in artery constriction.
    Keywords: Basic Science Research, Contractile Function, Vascular Biology, Hypertension, Pharmacology
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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