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
    Est1p as a cell cycle-regulated activator of telomere-bound telomerase (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-08-10
    Description: In Saccharomyces cerevisiae, the telomerase components Est2p, TLC1 RNA, Est1p, and Est3p are thought to form a complex that acts late during chromosome replication (S phase) upon recruitment by Cdc13p, a telomeric DNA binding protein. Consistent with this model, we show that Est1p, Est2p, and Cdc13p are telomere-associated at this time. However, Est2p, but not Est1p, also binds telomeres before late S phase. The cdc13-2 allele has been proposed to be defective in recruitment, yet Est1p and Est2p telomere association persists in cdc13-2 cells. These findings suggest a model in which Est1p binds telomeres late in S phase and interacts with Cdc13p to convert inactive, telomere-bound Est2p to an active form.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taggart, Andrew K P -- Teng, Shu-Chun -- Zakian, Virginia A -- GM43265/GM/NIGMS NIH HHS/ -- T32 CA09528-16/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Aug 9;297(5583):1023-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12169735" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; *Cell Cycle ; DNA, Fungal/genetics/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Enzyme Activation ; G1 Phase ; Genes, Fungal ; Models, Biological ; Polymerase Chain Reaction ; Precipitin Tests ; RNA, Fungal/genetics/metabolism ; S Phase ; Saccharomyces cerevisiae/cytology/enzymology/genetics/*metabolism ; Saccharomyces cerevisiae Proteins/genetics/*metabolism ; Telomerase/genetics/*metabolism ; Telomere/*metabolism ; *Telomere-Binding Proteins
    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
    Pif1p helicase, a catalytic inhibitor of telomerase in yeast (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-05
    Description: Mutations in the yeast Saccharomyces cerevisiae PIF1 gene, which encodes a 5'-to-3' DNA helicase, cause telomere lengthening and a large increase in the formation rate of new telomeres. Here, we show that Pif1p acts by inhibiting telomerase rather than telomere-telomere recombination, and this inhibition requires the helicase activity of Pif1p. Overexpression of enzymatically active Pif1p causes telomere shortening. Thus, Pif1p is a catalytic inhibitor of telomerase-mediated telomere lengthening. Because Pif1p is associated with telomeric DNA in vivo, its effects on telomeres are likely direct. Pif1p-like helicases are found in diverse organisms, including humans. We propose that Pif1p-mediated inhibition of telomerase promotes genetic stability by suppressing telomerase-mediated healing of double-strand breaks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, J -- Monson, E K -- Teng, S C -- Schulz, V P -- Zakian, V A -- GM26938/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Aug 4;289(5480):771-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, NJ 08544-1014, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10926538" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Motifs ; Animals ; Catalysis ; Cell Line ; Chromosomes, Fungal/metabolism ; DNA Damage ; DNA Helicases/chemistry/genetics/*metabolism ; DNA Replication ; DNA, Fungal/metabolism ; Gene Expression ; Humans ; Mutagenesis, Site-Directed ; Point Mutation ; Recombinant Proteins/chemistry/metabolism ; Recombination, Genetic ; Saccharomyces cerevisiae/*enzymology/genetics ; *Saccharomyces cerevisiae Proteins ; Sequence Homology, Amino Acid ; Telomerase/*antagonists & inhibitors/metabolism ; Telomere/*metabolism
    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
    Gender differences and performance in science (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, Carol B -- Ride, Sally M -- Fouke, Janie -- Whitney, Telle -- Denton, Denice D -- Cantor, Nancy -- Nelson, Donna J -- Plummer, Jim -- Busch-Vishniac, Ilene -- Meyers, Carolyn -- Rosser, Sue V -- Schiebinger, Londa -- Roberts, Eric -- Burgess, David -- Beeson, Craig -- Metz, Susan Staffin -- Sanders, Lucinda -- Watford, Bevlee A -- Ivey, Elizabeth S -- Frank Fox, Mary -- Wettack, Sheldon -- Klawe, Maria -- Wulf, William A -- Girgus, Joan -- Leboy, Phoebe S -- Babco, Eleanor L -- Shanahan, Betty -- Didion, Catherine -- Chubin, Daryl E -- Frize, Monique -- Ganter, Susan L -- Nalley, E Ann -- Franz, Judy -- Abruna, Hector D -- Strober, Myra H -- Zimmer Daniels, Jane -- Carter, Emily A -- Rhodes, Jean H -- Schrijver, Iris -- Zakian, Virginia A -- Simons, Barbara -- Martin, Ursula -- Boaler, Jo -- Jolluck, Katherine Rose -- Mankekar, Purnima -- Gray, Robert M -- Conkey, Margaret W -- Stansky, Peter -- Xie, Aihua -- Martin, Pino -- Katehi, Linda P B -- Miller, Jo Anne -- Tess Thornton, Amelia -- Lapaugh, Andrea -- Rhode, Deborah L -- Gelpi, Barbara C -- Harrold, Mary Jean -- Spencer, Cherrill M -- Schlatter Ellis, Carla -- Lord, Susan -- Quinn, Helen -- Murnane, Margaret -- Jones, Patricia P -- Hellman, Frances -- Wight, Gail -- O'hara, Ruth -- Pickering, Mary -- Sheppard, Sheri -- Leith, David -- Paytan, Adina -- Sommer, Matthew H -- Shafer, Audrey -- Grusky, David -- Yennello, Sherry -- Madan, Ashima -- Johnson, Denise L -- Yanagisako, Sylvia -- Chou-Green, Jennifer M -- Robinson, Sandra -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1043.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15718449" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Choice ; Female ; Humans ; Male ; *Science ; *Sex Characteristics ; Social Change
    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
  • 4
    facet.materialart.
    Unknown
    Expansion and length-dependent fragility of CTG repeats in yeast (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-28
    Description: Expansion of DNA trinucleotide repeats (TNRs) is the causative mutation in a growing number of human genetic diseases. Large expansions of a CTG tract were obtained and shown by genetic and physical assays to be length-dependent sites of chromosome breakage in Saccharomyces cerevisiae. Deletion of RAD27, which encodes a nuclease involved in Okazaki fragment processing, caused length-dependent destabilization of CTG tracts and a substantial increase in expansion frequency. The genetic assay described here can be used to evaluate other factors that induce TNR expansion or chromosome fragility in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freudenreich, C H -- Kantrow, S M -- Zakian, V A -- AG05740-02/AG/NIA NIH HHS/ -- GM26938/GM/NIGMS NIH HHS/ -- GM43265/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 6;279(5352):853-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9452383" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Breakage ; *Chromosome Fragility ; Chromosomes, Fungal/*metabolism ; DNA Damage ; DNA Repair ; DNA Replication ; DNA, Fungal/metabolism ; Electrophoresis, Gel, Pulsed-Field ; Exodeoxyribonuclease V ; Exodeoxyribonucleases/genetics ; Gene Deletion ; Genes, Fungal ; Humans ; Hydroxyurea/pharmacology ; Recombination, Genetic ; Saccharomyces cerevisiae/*genetics/metabolism ; Transformation, Genetic ; *Trinucleotide Repeat Expansion ; Trinucleotide Repeats/*genetics
    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
  • 5
    facet.materialart.
    Unknown
    Pif1 family helicases suppress genome instability at G-quadruplex motifs (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-05-10
    Description: The Saccharomyces cerevisiae Pif1 helicase is the prototypical member of the Pif1 DNA helicase family, which is conserved from bacteria to humans. Here we show that exceptionally potent G-quadruplex unwinding is conserved among Pif1 helicases. Moreover, Pif1 helicases from organisms separated by more than 3 billion years of evolution suppressed DNA damage at G-quadruplex motifs in yeast. The G-quadruplex-induced damage generated in the absence of Pif1 helicases led to new genetic and epigenetic changes. Furthermore, when expressed in yeast, human PIF1 suppressed both G-quadruplex-associated DNA damage and telomere lengthening.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3680789/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3680789/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paeschke, Katrin -- Bochman, Matthew L -- Garcia, P Daniela -- Cejka, Petr -- Friedman, Katherine L -- Kowalczykowski, Stephen C -- Zakian, Virginia A -- R01 GM026938/GM/NIGMS NIH HHS/ -- R01 GM041347/GM/NIGMS NIH HHS/ -- R01 GM043265/GM/NIGMS NIH HHS/ -- England -- Nature. 2013 May 23;497(7450):458-62. doi: 10.1038/nature12149. Epub 2013 May 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23657261" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Conserved Sequence ; DNA Damage/genetics ; DNA Helicases/deficiency/genetics/*metabolism ; Epigenesis, Genetic ; Evolution, Molecular ; *G-Quadruplexes ; Gene Silencing ; Genetic Complementation Test ; *Genomic Instability ; Humans ; Molecular Sequence Data ; Mutation Rate ; Saccharomyces cerevisiae/*genetics/*metabolism ; Saccharomyces cerevisiae Proteins/genetics ; Telomere Homeostasis/genetics
    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
  • 6
    facet.materialart.
    Unknown
    Telomeres: beginning to understand the end (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-12-08
    Description: Telomeres are the protein-DNA structures at the ends of eukaryotic chromosomes. In yeast, and probably most other eukaryotes, telomeres are essential. They allow the cell to distinguish intact from broken chromosomes, protect chromosomes from degradation, and are substrates for novel replication mechanisms. Telomeres are usually replicated by telomerase, a telomere-specific reverse transcriptase, although telomerase-independent mechanisms of telomere maintenance exist. Telomere replication is both cell cycle- and developmentally regulated, and its control is likely to be complex. Because telomere loss causes the kinds of chromosomal changes associated with cancer and aging, an understanding of telomere biology has medical relevance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zakian, V A -- New York, N.Y. -- Science. 1995 Dec 8;270(5242):1601-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, NJ 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7502069" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Cycle ; Chromosomes/metabolism/physiology ; DNA/analysis/chemistry/metabolism ; DNA Replication ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation ; Humans ; Molecular Sequence Data ; Telomerase/metabolism ; Telomere/chemistry/*physiology
    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
  • 7
    facet.materialart.
    Unknown
    Ciliates: the molecular biology of ciliated protozoa (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zakian, V A -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):306.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17772061" target="_blank"〉PubMed〈/a〉
    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
  • 8
    Electronic Resource
    Electronic Resource
    Structure and Function of Telomeres (1989)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Genetics 23 (1989), S. 579-604 
    Details
    ISSN: 0066-4197
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.ge.23.120189.003051
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Accelerated loss of telomeric repeats may not explain accelerated replicative decline of Werner syndrome cells (1996)
    Springer
    Human genetics 〈Berlin〉 97 (1996), S. 750-754 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The Werner syndrome (WS) is characterized by the premature onset and accelerated rates of development of major geriatric disorders, including atherosclerosis, diabetes mellitus, osteoporosis, ocular cataracts, and various neoplasms. Cultures of WS skin-fibroblastlike cells have been previously shown to undergo accelerated rates of decline of their replicative potentials and to exhibit variegated chromosomal translocations and deletions. Since the replicative decline of normal somatic cells is associated with a loss of telomeric repeats, we investigated the kinetics of telomeric repeat loss in WS cells. The mean length of telomere restriction fragments (TRF) from the earliest passages of WS cells studied was not shorter than those of controls, possibly reflecting selective pressure for subsets of cells with relatively high residual replicative capacity. Statistical evidence indicated an accelerated shortening of TRF length in serially passaged WS cultures, but the mean TRF lengths of WS cultures that had ceased replicating were significantly longer than those of senescent controls. Thus, while accelerated loss of telomeric repeats could potentially explain the rapid decline in proliferation of WS cells, it is possible that WS cells exit the cell cycle via mechanisms that differ from those of replicatively senescent cells from control subjects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004390050131
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Accelerated loss of telomeric repeats may not explain accelerated replicative decline of Werner syndrome cells (1996)
    Springer
    Human genetics 〈Berlin〉 97 (1996), S. 750-754 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The Werner syndrome (WS) is characterized by the premature onset and accelerated rate of development of major geriatric disorders, including atherosclerosis, diabetes mellitus, osteoporosis, ocular cataracts, and various neoplasms. Cultures of WS skin-fibroblastlike cells have been previously shown to undergo accelerated rates of decline of their replicative potentials and to exhibit variegated chromosomal translocations and deletions. Since the replicative decline of normal somatic cells is associated with a loss of telomeric repeats, we investigated the kinetics of telomeric repeat loss in WS cells. The mean length of telomere restriction fragments (TRF) from the earliest passages of WS cells studied was not shorter than those of controls, possibly reflecting selective pressure for subsets of cells with relatively high residual replicative capacity. Statistical evidence indicated an accelerated shortening of TRF length in serially passaged WS cultures, but the mean TRF lengths of WS cultures that had ceased replicating were significantly longer than those of senescent controls. Thus, while accelerated loss of telomeric repeats could potentially explain the rapid decline in proliferation of WS cells, it is possible that WS cells exit the cell cycle via mechanisms that differ from those of replicatively senescent cells from control subjects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02346184
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...