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  • 1
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    T cell memory. Skin-resident memory CD8(+) T cells trigger a state of tissue-wide pathogen alert (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-10-04
    Description: After an infection, pathogen-specific tissue-resident memory T cells (T(RM) cells) persist in nonlymphoid tissues to provide rapid control upon reinfection, and vaccination strategies that create T(RM) cell pools at sites of pathogen entry are therefore attractive. However, it is not well understood how T(RM) cells provide such pathogen protection. Here, we demonstrate that activated T(RM) cells in mouse skin profoundly alter the local tissue environment by inducing a number of broadly active antiviral and antibacterial genes. This "pathogen alert" allows skin T(RM) cells to protect against an antigenically unrelated virus. These data describe a mechanism by which tissue-resident memory CD8(+) T cells protect previously infected sites that is rapid, amplifies the activation of a small number of cells into an organ-wide response, and has the capacity to control escape variants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ariotti, Silvia -- Hogenbirk, Marc A -- Dijkgraaf, Feline E -- Visser, Lindy L -- Hoekstra, Mirjam E -- Song, Ji-Ying -- Jacobs, Heinz -- Haanen, John B -- Schumacher, Ton N -- New York, N.Y. -- Science. 2014 Oct 3;346(6205):101-5. doi: 10.1126/science.1254803. Epub 2014 Aug 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Division of Biological Stress Response, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Experimental Animal Pathology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Division of Immunology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. t.schumacher@nki.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25278612" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/*immunology ; Female ; Immunologic Memory/genetics/*immunology ; Male ; Mice ; Skin/*immunology/microbiology/virology ; Transcriptome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Direct determinants of chromosomal translocations [Biophysics and Computational Biology] (2016)
    National Academy of Sciences
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    Publication Date: 2016-06-30
    Description: Chromosomal translocations are a hallmark of cancer. Unraveling the molecular mechanism of these rare genetic events requires a clear distinction between correlative and causative risk-determinants, where technical and analytical issues can be excluded. To meet this goal, we performed in-depth analyses of publicly available genome-wide datasets. In contrast to several...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 3
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    Roles of PCNA ubiquitination and TLS polymerases {kappa} and {eta} in the bypass of methyl methanesulfonate-induced DNA damage (2015)
    Oxford University Press
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    Publication Date: 2015-01-10
    Description: Translesion synthesis (TLS) provides a highly conserved mechanism that enables DNA synthesis on a damaged template. TLS is performed by specialized DNA polymerases of which polymerase (Pol) is important for the cellular response to DNA damage induced by benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE), ultraviolet (UV) light and the alkylating agent methyl methanesulfonate (MMS). As TLS polymerases are intrinsically error-prone, tight regulation of their activity is required. One level of control is provided by ubiquitination of the homotrimeric DNA clamp PCNA at lysine residue 164 (PCNA-Ub). We here show that Pol can function independently of PCNA modification and that Pol can function as a backup during TLS of MMS-induced lesions. Compared to cell lines deficient for PCNA modification ( Pcna K164R ) or Pol, double mutant cell lines display hypersensitivity to MMS but not to BPDE or UV-C. Double mutant cells also displayed delayed post-replicative TLS, accumulate higher levels of replication stress and delayed S-phase progression. Furthermore, we show that Pol and Pol are redundant in the DNA damage bypass of MMS-induced DNA damage. Taken together, we provide evidence for PCNA-Ub-independent activation of Pol and establish Pol as an important backup polymerase in the absence of Pol in response to MMS-induced DNA damage.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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