ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Ku70 corrupts DNA repair in the absence of the Fanconi anemia pathway (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-12
    Description: A conserved DNA repair response is defective in the human genetic illness Fanconi anemia (FA). Mutation of some FA genes impairs homologous recombination and error-prone DNA repair, rendering FA cells sensitive to DNA cross-linking agents. We found a genetic interaction between the FA gene FANCC and the nonhomologous end joining (NHEJ) factor Ku70. Disruption of both FANCC and Ku70 suppresses sensitivity to cross-linking agents, diminishes chromosome breaks, and reverses defective homologous recombination. Ku70 binds directly to free DNA ends, committing them to NHEJ repair. We show that purified FANCD2, a downstream effector of the FA pathway, might antagonize Ku70 activity by modifying such DNA substrates. These results reveal a function for the FA pathway in processing DNA ends, thereby diverting double-strand break repair away from abortive NHEJ and toward homologous recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pace, Paul -- Mosedale, Georgina -- Hodskinson, Michael R -- Rosado, Ivan V -- Sivasubramaniam, Meera -- Patel, Ketan J -- MC_U105178811/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 9;329(5988):219-23. doi: 10.1126/science.1192277. Epub 2010 Jun 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20538911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Nuclear/*genetics/metabolism ; Cell Line ; Chickens ; Chromosome Breakage ; Cross-Linking Reagents/pharmacology ; *DNA Breaks, Double-Stranded ; *DNA Repair ; DNA-Binding Proteins/*genetics/metabolism ; Fanconi Anemia Complementation Group C Protein/*genetics/metabolism ; Fanconi Anemia Complementation Group D2 Protein/chemistry/genetics/*metabolism ; Gene Conversion ; Genes, Immunoglobulin ; Humans ; Immunoglobulin M/genetics ; Point Mutation ; Recombinant Proteins/metabolism ; *Recombination, Genetic
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Retrospective. Michael Neuberger (1953-2013) (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sale, Julian E -- Patel, Ketan J -- Batista, Facundo D -- MC_U105178808/Medical Research Council/United Kingdom -- MC_U105178811/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Dec 13;342(6164):1335. doi: 10.1126/science.1248808.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24337288" target="_blank"〉PubMed〈/a〉
    Keywords: Allergy and Immunology/*history ; Animals ; Antibodies, Monoclonal, Humanized/*history ; *Antibody Diversity ; Biomedical Engineering/*history ; Great Britain ; History, 20th Century ; History, 21st Century ; Humans ; Mice ; Molecular Biology/*history
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Fancd2 counteracts the toxic effects of naturally produced aldehydes in mice (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-07-08
    Description: Reactive aldehydes are common carcinogens. They are also by-products of several metabolic pathways and, without enzymatic catabolism, may accumulate and cause DNA damage. Ethanol, which is metabolised to acetaldehyde, is both carcinogenic and teratogenic in humans. Here we find that the Fanconi anaemia DNA repair pathway counteracts acetaldehyde-induced genotoxicity in mice. Our results show that the acetaldehyde-catabolising enzyme Aldh2 is essential for the development of Fancd2(-/-) embryos. Nevertheless, acetaldehyde-catabolism-competent mothers (Aldh2(+/-)) can support the development of double-mutant (Aldh2(-/-)Fancd2(-/-)) mice. However, these embryos are unusually sensitive to ethanol exposure in utero, and ethanol consumption by postnatal double-deficient mice rapidly precipitates bone marrow failure. Lastly, Aldh2(-/-)Fancd2(-/-) mice spontaneously develop acute leukaemia. Acetaldehyde-mediated DNA damage may critically contribute to the genesis of fetal alcohol syndrome in fetuses, as well as to abnormal development, haematopoietic failure and cancer predisposition in Fanconi anaemia patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langevin, Frederic -- Crossan, Gerry P -- Rosado, Ivan V -- Arends, Mark J -- Patel, Ketan J -- MC_U105178811/Medical Research Council/United Kingdom -- England -- Nature. 2011 Jul 6;475(7354):53-8. doi: 10.1038/nature10192.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21734703" target="_blank"〉PubMed〈/a〉
    Keywords: Acetaldehyde/metabolism/toxicity ; Aldehyde Dehydrogenase/deficiency/genetics/metabolism ; Aldehydes/*antagonists & inhibitors/metabolism/*toxicity ; Alleles ; Animals ; B-Lymphocytes/drug effects/metabolism ; Bone Marrow/drug effects/pathology/physiopathology ; Cell Line ; Cell Survival/drug effects ; Chickens ; Clone Cells/drug effects ; DNA Damage/genetics ; DNA Repair/genetics ; Embryo Loss/chemically induced/etiology ; Embryo, Mammalian/abnormalities/drug effects/embryology ; Ethanol/metabolism/toxicity ; Fanconi Anemia/genetics/pathology ; Fanconi Anemia Complementation Group D2 Protein/deficiency/genetics/*metabolism ; Female ; Fetal Alcohol Spectrum Disorders/etiology ; Gene Deletion ; Genes, Essential ; Hematopoiesis/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/chemically induced/etiology ; Pregnancy ; Teratogens/metabolism/toxicity ; Weaning
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Genotoxic consequences of endogenous aldehydes on mouse haematopoietic stem cell function (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-08-28
    Description: Haematopoietic stem cells (HSCs) regenerate blood cells throughout the lifespan of an organism. With age, the functional quality of HSCs declines, partly owing to the accumulation of damaged DNA. However, the factors that damage DNA and the protective mechanisms that operate in these cells are poorly understood. We have recently shown that the Fanconi anaemia DNA-repair pathway counteracts the genotoxic effects of reactive aldehydes. Mice with combined inactivation of aldehyde catabolism (through Aldh2 knockout) and the Fanconi anaemia DNA-repair pathway (Fancd2 knockout) display developmental defects, a predisposition to leukaemia, and are susceptible to the toxic effects of ethanol-an exogenous source of acetaldehyde. Here we report that aged Aldh2(-/-) Fancd2(-/-) mutant mice that do not develop leukaemia spontaneously develop aplastic anaemia, with the concomitant accumulation of damaged DNA within the haematopoietic stem and progenitor cell (HSPC) pool. Unexpectedly, we find that only HSPCs, and not more mature blood precursors, require Aldh2 for protection against acetaldehyde toxicity. Additionally, the aldehyde-oxidizing activity of HSPCs, as measured by Aldefluor stain, is due to Aldh2 and correlates with this protection. Finally, there is more than a 600-fold reduction in the HSC pool of mice deficient in both Fanconi anaemia pathway-mediated DNA repair and acetaldehyde detoxification. Therefore, the emergence of bone marrow failure in Fanconi anaemia is probably due to aldehyde-mediated genotoxicity restricted to the HSPC pool. These findings identify a new link between endogenous reactive metabolites and DNA damage in HSCs, and define the protective mechanisms that counteract this threat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garaycoechea, Juan I -- Crossan, Gerry P -- Langevin, Frederic -- Daly, Maria -- Arends, Mark J -- Patel, Ketan J -- MC_U105178811/Medical Research Council/United Kingdom -- England -- Nature. 2012 Sep 27;489(7417):571-5. doi: 10.1038/nature11368. Epub 2012 Aug 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22922648" target="_blank"〉PubMed〈/a〉
    Keywords: Acetaldehyde/metabolism/toxicity ; Aging ; Aldehyde Dehydrogenase/deficiency/genetics/metabolism ; Aldehydes/metabolism/*toxicity ; Animals ; Bone Marrow/pathology ; DNA Damage/drug effects/genetics ; DNA Repair ; Ethanol/toxicity ; Fanconi Anemia/pathology ; Fanconi Anemia Complementation Group D2 Protein/deficiency/genetics ; Female ; Hematopoietic Stem Cells/*cytology/*drug effects/enzymology/metabolism ; Kaplan-Meier Estimate ; Leukemia/metabolism/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutagens/*toxicity
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Studies of ZrO2 electrolyte thin-film thickness on the all-solid thin-film electrochromic devices (2014)
    Springer
    Details
    Publication Date: 2014-08-08
    Print ISSN: 1432-8488
    Electronic ISSN: 1433-0768
    Topics: Chemistry and Pharmacology
    Published by Springer
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Abundance of the Fanconi anaemia core complex is regulated by the RuvBL1 and RuvBL2 AAA+ ATPases (2014)
    Oxford University Press
    Details
    Publication Date: 2014-12-17
    Description: Fanconi anaemia (FA) is a genome instability disease caused by defects in the FA DNA repair pathway that senses and repairs damage caused by DNA interstrand crosslinks. At least 8 of the 16 genes found mutated in FA encode proteins that assemble into the FA core complex, a multisubunit monoubiquitin E3 ligase. Here, we show that the RuvBL1 and RuvBL2 AAA+ ATPases co-purify with FA core complex isolated under stringent but native conditions from a vertebrate cell line. Depletion of the RuvBL1-RuvBL2 complex in human cells causes hallmark features of FA including DNA crosslinker sensitivity, chromosomal instability and defective FA pathway activation. Genetic knockout of RuvBL1 in a murine model is embryonic lethal while conditional inactivation in the haematopoietic stem cell pool confers profound aplastic anaemia. Together these findings reveal a function for RuvBL1-RuvBL2 in DNA repair through a physical and functional association with the FA core complex. Surprisingly, depletion of RuvBL1-RuvBL2 leads to co-depletion of the FA core complex in human cells. This suggests that a potential mechanism for the role of RuvBL1-RuvBL2 in maintaining genome integrity is through controlling the cellular abundance of FA core complex.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    The alpha/beta sheath and its cytoplasmic tyrosines are required for signaling by the B-cell antigen receptor but not for capping or for serine/threonine-kinase recruitment. (1994)
    National Academy of Sciences
    Details
    Publication Date: 1994-01-18
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    FANCJ coordinates two pathways that maintain epigenetic stability at G-quadruplex DNA (2012)
    Oxford University Press
    Details
    Publication Date: 2012-02-28
    Description: We have previously reported that DT40 cells deficient in the Y-family polymerase REV1 are defective in replicating G-quadruplex DNA. In vivo this leads to uncoupling of DNA synthesis from redeposition of histones displaced ahead of the replication fork, which in turn leads to loss of transcriptional repression due to failure to recycle pre-existing repressive histone post-translational modifications. Here we report that a similar process can also affect transcriptionally active genes, leading to their deactivation. We use this finding to develop an assay based on loss of expression of a cell surface marker to monitor epigenetic instability at the level of single cells. This assay allows us to demonstrate G4 DNA motif-associated epigenetic instability in mutants of three helicases previously implicated in the unwinding of G-quadruplex structures, FANCJ, WRN and BLM. Transcriptional profiling of DT40 mutants reveals that FANCJ coordinates two independent mechanisms to maintain epigenetic stability near G4 DNA motifs that are dependent on either REV1 or on the WRN and BLM helicases, suggesting a model in which efficient in vivo replication of G-quadruplexes often requires the established 5'–3'-helicase activity of FANCJ acting in concert with either a specialized polymerase or helicase operating in the opposite polarity.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    Of sizzling steaks and DNA repair (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-07-14
    Keywords: Physics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    All-inorganic solid-state electrochromic devices: a review (2016)
    Springer
    Details
    Publication Date: 2016-09-28
    Print ISSN: 1432-8488
    Electronic ISSN: 1433-0768
    Topics: Chemistry and Pharmacology
    Published by Springer
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...