157 research outputs found
IR Bismuth active centers in optical fibers: Combined excitation-emission spectroscopy
3D excitation-emission luminescence spectra of Bi-doped optical fibers of
various compositions were measured in a wide wavelength range 450-1700 nm. Such
luminescence spectra were obtained for Bi-doped pure silica and germania
fibers, and for Bi-doped Al- or P-codoped silica fibers (at room and liquid
nitrogen temperatures). The energy level schemes of IR bismuth active centers
in pure silica and germania core fibers were derived from spectra obtained. The
energy level schemes similarity of bismuth active centers in these two types of
fibers was revealed.Comment: 12pages, 7 figures, 5 table
USP7/HAUSP stimulates repair of oxidative DNA lesions
USP7 is involved in the cellular stress response by regulating Mdm2 and p53 protein levels following severe DNA damage. In addition to this, USP7 may also play a role in chromatin remodelling by direct deubiquitylation of histones, as well as indirectly by regulating the cellular levels of E3 ubiquitin ligases involved in histone ubiquitylation. Here, we provide new evidence that USP7 modulated chromatin remodelling is important for base excision repair of oxidative lesions. We show that transient USP7 siRNA knockdown did not change the levels or activity of base excision repair enzymes, but significantly reduced chromatin DNA accessibility and consequently the rate of repair of oxidative lesions
Luminescent properties of Bi-doped polycrystalline KAlCl4
We observed an intensive near-infrared luminescence in Bi-doped KAlCl4
polycrystalline material. Luminescence dependence on the excitation wavelength
and temperature of the sample was studied. Our experimental results allow
asserting that the luminescence peaked near 1 um belongs solely to Bi+ ion
which isomorphically substitutes potassium in the crystal. It was also
demonstrated that Bi+ luminescence features strongly depend on the local ion
surroundings
UVSSA and USP7, a new couple in transcription-coupled DNA repair
Transcription-coupled nucleotide excision repair (TC-NER) specifically removes transcription-blocking lesions from our genome. Defects in this pathway are associated with two human disorders: Cockayne syndrome (CS) and UV-sensitive syndrome (UVSS). Despite a similar cellular defect in the UV DNA damage response, patients with these syndromes exhibit strikingly distinct symptoms; CS patients display severe developmental, neurological, and premature aging features, whereas the phenotype of UVSS patients is mostly restricted to UV hypersensitivity. The exact molecular mechanism behind these clinical differences is still unknown; however, they might be explained by additional functions of CS proteins beyond TC-NER. A short overview of the current hypotheses addressing possible molecular mechanisms and the proteins involved are presented in this review. In addition, we will focus on two new players involved in TC-NER which were recently identified: UV-stimulated scaffold protein A (UVSSA) and ubiquitin-specific protease 7 (USP7). UVSSA has been found to be the causative gene for UVSS and, together with USP7, is implicated in regulating TC-NER activity. We will discuss the function of UVSSA and USP7 and how the discovery of these proteins contributes to a better understanding of the molecular mechanisms underlying the clinical differences between UVSS and the more severe CS
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