963 resultados para ULTRAVIOLET PHOTODETECTOR
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Xeroderma pigmentosum type G (XPG) is a human genetic disease exhibiting extreme sensitivity to sunlight. XPG patients are defective XPG endonuclease, which is an enzyme essential for DNA repair of the major kinds of solar ultraviolet (UV)-induced DNA damages. Here we describe a novel dynamics of this protein within the cell nucleus after UV irradiation of human cells. Using confocal microscopy, we have localized the immunofluorescent, antigenic signal of XPG protein to foci throughout the cell nucleus. Our biochemical studies also established that XPG protein forms a tight association with nuclear structure(s). In human skin fibroblast cells, the number of XPG foci decreased within 2 h after UV irradiation, whereas total nuclear XPG fluorescence intensity remained constant, suggesting redistribution of XPG from a limited number of nuclear foci to the nucleus overall. Within 8 h after UV, most XPG antigenic signal was found as foci. Using beta-galactosidase-XPG fusion constructs (beta-gal-XPG) transfected into HeLa cells, we have identified a single region of XPG that is evidently responsible both for foci formation and for the UV dynamic response. The fusion protein carrying the C terminus of XPG (amino acids 1146-1185) localized beta-gal specific antigenic signal to foci and to the nucleolus regions. After UV irradiation, antigenic beta-gal translocated reversibly from the subnuclear structures to the whole nucleus with kinetics very similar to the movements of XPG protein. These findings lead us to propose a model in which distribution of XPG protein may regulate the rate of DNA repair within transcriptionally active and inactive compartments of the cell nucleus.
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A combination of psoralen and ultraviolet A radiation (PUVA) is widely used in the treatment of psoriasis. However, PUVA treatment increases the risk of developing skin cancer in psoriasis patients and induces skin cancer in mice. Since the DNA damage induced by PUVA is quite different from that induced by UV, we investigated whether PUVA-induced mouse skin cancers display carcinogen-specific mutations in the p53 tumor suppressor gene. The results indicated that 10 of 13 (77%) PUVA-induced skin tumors contained missense mutations predominantly at exons 6 and 7. In contrast, tumor-adjacent, PUVA-exposed skin from tumor-bearing animals did not exhibit p53 mutation in exons 4-8. Interestingly, about 40% of all mutations in PUVA-induced skin tumors occurred at 5'-TA sites, and an equal number of mutations occurred at one base flanking 5'TA or 5'-TAT sites. Since PUVA induces DNA cross-links exclusively at these sites and since UV "signature" mutations were rarely detected in PUVA-induced skin cancers, we can conclude that PUVA acts as a carcinogen by inducing unique PUVA signature mutations in p53. This finding may have implications for identifying the etiology of skin cancer in psoriasis patients who have undergone PUVA therapy.
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Cyanobacteria are important contributors to global photosynthesis in both marine and terrestrial environments. Quantitative data are presented on UV-B-induced damage to the major cyanobacterial photosynthetic light harvesting complex, the phycobilisome, and to each of its constituent phycobiliproteins. The photodestruction quantum yield, phi295 nm, for the phycobiliproteins is high (approximately 10(-3), as compared with approximately 10(-7) for visible light). Energy transfer on a picosecond time scale does not compete with photodestruction. Photodamage to phycobilisomes in vitro and in living cells is amplified by causing dissociation and loss of function of the complex. In photosynthetic organisms, UV-B damage to light-harvesting complexes may significantly exceed that to DNA.
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Acknowledgements This work was supported by NSF DMR-1410378 and DMR-1121288. We thank V. Borshch for helping with preparation of illustrations, to Y. K. Kim for the help in experiments, V. A. Belyakov and S. V. Shiyanovskii for useful discussions.
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We present high-resolution optical echelle spectra and IUE observations during a strong flare on 1993 December 22 in the very active, young, rapidly rotating, single K2 dwarf LQ Hya. The initial impulsive phase of the flare, which started sometime between 2:42 ut and 4:07 ut, was characterized by strong optical continuum enhancement and blueshifted emission lines with broad wings. The optical chromospheric lines reached their maximum intensity at ≈ 5:31 ut, by which time the blueshift vanished and the optical continuum enhancement had sharply decreased. Thereafter, the line emission slowly decreased and the lines redshift in a gradual phase that lasted at least two more hours. The Mg II lines behaved similarly. Quiescent C IV flux levels were not recovered until 21 h later, though a data gap and a possible second flare make the interpretation uncertain. In addition to the typically flare-enhanced emission lines (e.g., H α and H β), we observe He I D_3 going into emission, plus excess emission (after subtraction of the quiescent spectrum) in other He I and several strong neutral metal lines (e.g., Mg I b). Flare enhancement of the far-ultraviolet continuum generally agrees with an Si I recombination model. We estimate the total flare energy, and discuss the broad components, asymmetries and Doppler shifts seen in some of the emission lines.
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Mode of access: Internet.
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Mode of access: Internet.
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Mode of access: Internet.
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Reprinted from the Physical review n.s. v.18, no.6. Dec.1921.
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Mode of access: Internet.
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Mode of access: Internet.
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Mode of access: Internet.
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Thesis (Master's)--University of Washington, 2016-06