18 research outputs found

    Zur ethnologie der inselkette zwischen Luzon und Formosa /

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    "Wiederabdruck nur mit angabe der quelle gestattet.""Sonderabdruck ans den 'Vittellungen' der Deutschen gesellschaft fūr natur- und vōlkerkunde Ostasiens, bd. XI, teil 1."cover-titleMode of access: Internet.Author's autograph presentation copy to Dean C. Worceste

    Título: The Bataks of Palawan

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    Índic

    The Nabaloi dialect

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    Índic

    Part I: Batan dialect as member of Philippine group of languages. Part II: F and V in Philippine languages [comparisons of dialects].

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    Batan dialect as member of Philippine group of languages; "F" and "V" in Philippine languages.CIS Index to U. S. Executive Branch Documents, 1789-1909, Part 2.Microfiche.Mode of access: Internet

    The Nabaloi dialect /

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    "The Ibaloi Igorot seventy-five years ago : account of a Spanish expedition to Benguet in the year 1829 ; translated from Informe sobre el estado de las islas Filipinas en 1842 (by S. Mas), Madrid, 1842: Diary of Don G. Galvey, in command of the forces for the suppression of contraband trade": p. 173-178."Nabaloi vocabulary": p. 151-171.With music (Ibaloi melodies)Includes index.CIS Index to U. S. Executive Branch Documents, 1789-1909, Part 2.Microfiche.Mode of access: Internet

    A Polarity Probe for Monitoring Light-induced Structural Changes at the Entrance of the Chromophore Pocket in a Bacterial Phytochrome*

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    Light-induced structural changes at the entrance of the chromophore pocket of Agp1 phytochrome were investigated by using a thiol-reactive fluorescein derivative that is covalently attached to the genuine chromophore binding site (Cys-20) and serves as a polarity probe. In the apoprotein, the absorption spectrum of bound fluorescein is red-shifted with respect to that of the free label suggesting that the probe enters the hydrophobic chromophore pocket. Assembly of this construct with the chromophores phycocyanobilin or biliverdin is associated with a blue-shift of the fluorescein absorption band indicating the displacement of the probe out of the pocket. The probe does not affect the photochromic and kinetic properties of the noncovalent bilin adducts. Upon photoconversion to Pfr, the probe spectrum undergoes again a bathochromic shift and a strong rise in CD indicating a more hydrophobic and asymmetric environment. We propose that the environmental changes of the probe reflect conformational changes at the entrance of the chromophore pocket and are indicative for rearrangements of the chromophore ring A. Flash photolysis measurements showed that the absorption changes of the probe are kinetically coupled to the formation of Meta-RC and Pfr. In the biliverdin adduct, an additional component occurs that probably reflects a transition between two Meta-RC substates. Analogous results to that of the noncovalent phycocyanobilin adduct were obtained with the mutant V249C in which probe and chromophore are covalently attached. The conformational changes of the chromophore are correlated to proton transfer to the protein surface

    Aurora kinases A and B are up-regulated by Myc and are essential for maintenance of the malignant state

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    Myc oncoproteins promote continuous cell growth, in part by controlling the transcription of key cell cycle regulators. Here, we report that c-Myc regulates the expression of Aurora A and B kinases (Aurka and Aurkb), and that Aurka and Aurkb transcripts and protein levels are highly elevated in Myc-driven B-cell lymphomas in both mice and humans. The induction of Aurka by Myc is transcriptional and is directly mediated via E-boxes, whereas Aurkb is regulated indirectly. Blocking Aurka/b kinase activity with a selective Aurora kinase inhibitor triggers transient mitotic arrest, polyploidization, and apoptosis of Myc-induced lymphomas. These phenotypes are selectively bypassed by a kinase inhibitor-resistant Aurkb mutant, demonstrating that Aurkb is the primary therapeutic target in the context of Myc. Importantly, apoptosis provoked by Aurk inhibition was p53 independent, suggesting that Aurka/Aurkb inhibitors will show efficacy in treating primary or relapsed malignancies having Myc involvement and/or loss of p53 function
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