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  • 1
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    Low levels of aneuploidy across mammalian tissues [Genetics] (2014)
    National Academy of Sciences
    Details
    Publication Date: 2014-09-17
    Description: Whole-chromosome copy number alterations, also known as aneuploidy, are associated with adverse consequences in most cells and organisms. However, high frequencies of aneuploidy have been reported to occur naturally in the mammalian liver and brain, fueling speculation that aneuploidy provides a selective advantage in these organs. To explore this paradox,...
    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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  • 2
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    Path selection rules for droplet trains in single-lane microfluidic networks (2013)
    American Physical Society (APS)
    Details
    Publication Date: 2013-07-19
    Description: Author(s): A. Amon, A. Schmit, L. Salkin, L. Courbin, and P. Panizza We investigate the transport of periodic trains of droplets through microfluidic networks having one inlet, one outlet, and nodes consisting of T junctions. Variations of the dilution of the trains, i.e., the distance between drops, reveal the existence of various hydrodynamic regimes characterized ... [Phys. Rev. E 88, 013012] Published Thu Jul 18, 2013
    Keywords: Fluid Dynamics
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
    Topics: Physics
    Published by American Physical Society (APS)
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  • 3
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    Cell biology: the micronucleus gets its big break (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-05-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knouse, Kristin A -- Amon, Angelika -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2015 Jun 11;522(7555):162-3. doi: 10.1038/nature14528. Epub 2015 May 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Koch Institute for Integrative Cancer Research, Department of Biology, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26017308" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Breakage ; *DNA Damage ; Humans ; *Micronuclei, Chromosome-Defective
    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)
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  • 4
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    Effects of aneuploidy on cellular physiology and cell division in haploid yeast (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-19
    Description: Aneuploidy is a condition frequently found in tumor cells, but its effect on cellular physiology is not known. We have characterized one aspect of aneuploidy: the gain of extra chromosomes. We created a collection of haploid yeast strains that each bear an extra copy of one or more of almost all of the yeast chromosomes. Their characterization revealed that aneuploid strains share a number of phenotypes, including defects in cell cycle progression, increased glucose uptake, and increased sensitivity to conditions interfering with protein synthesis and protein folding. These phenotypes were observed only in strains carrying additional yeast genes, which indicates that they reflect the consequences of additional protein production as well as the resulting imbalances in cellular protein composition. We conclude that aneuploidy causes not only a proliferative disadvantage but also a set of phenotypes that is independent of the identity of the individual extra chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Torres, Eduardo M -- Sokolsky, Tanya -- Tucker, Cheryl M -- Chan, Leon Y -- Boselli, Monica -- Dunham, Maitreya J -- Amon, Angelika -- GM071508/GM/NIGMS NIH HHS/ -- GM56800/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 17;317(5840):916-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, E17-233, 40 Ames Street, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17702937" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Cell Division ; *Cell Proliferation ; Chromosomes, Fungal/genetics ; G1 Phase ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Glucose/metabolism ; Haploidy ; Phenotype ; Protein Synthesis Inhibitors/pharmacology ; Saccharomyces cerevisiae/cytology/*genetics/*physiology ; Saccharomyces cerevisiae Proteins/biosynthesis/metabolism ; Temperature ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Gametogenesis eliminates age-induced cellular damage and resets life span in yeast (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-28
    Description: Eukaryotic organisms age, yet detrimental age-associated traits are not passed on to progeny. How life span is reset from one generation to the next is not known. We show that in budding yeast resetting of life span occurs during gametogenesis. Gametes (spores) generated by aged cells show the same replicative potential as gametes generated by young cells. Age-associated damage is no longer detectable in mature gametes. Furthermore, transient induction of a transcription factor essential for later stages of gametogenesis extends the replicative life span of aged cells. Our results indicate that gamete formation brings about rejuvenation by eliminating age-induced cellular damage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3923466/" 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/PMC3923466/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Unal, Elcin -- Kinde, Benyam -- Amon, Angelika -- GM62207/GM/NIGMS NIH HHS/ -- R01 GM056800/GM/NIGMS NIH HHS/ -- R01 GM056800-17/GM/NIGMS NIH HHS/ -- R01 GM062207/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Jun 24;332(6037):1554-7. doi: 10.1126/science.1204349.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21700873" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Cell Division ; Cell Nucleolus/physiology/ultrastructure ; DNA, Circular/genetics/metabolism ; DNA, Fungal/genetics/metabolism ; DNA, Ribosomal/genetics/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Heat-Shock Proteins/metabolism ; Meiosis ; Nuclear Proteins/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/genetics/growth & development/*physiology/ultrastructure ; Saccharomyces cerevisiae Proteins/genetics/*metabolism ; Spores, Fungal/*physiology ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Aneuploidy drives genomic instability in yeast (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-20
    Description: Aneuploidy decreases cellular fitness, yet it is also associated with cancer, a disease of enhanced proliferative capacity. To investigate one mechanism by which aneuploidy could contribute to tumorigenesis, we examined the effects of aneuploidy on genomic stability. We analyzed 13 budding yeast strains that carry extra copies of single chromosomes and found that all aneuploid strains exhibited one or more forms of genomic instability. Most strains displayed increased chromosome loss and mitotic recombination, as well as defective DNA damage repair. Aneuploid fission yeast strains also exhibited defects in mitotic recombination. Aneuploidy-induced genomic instability could facilitate the development of genetic alterations that drive malignant growth in cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278960/" 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/PMC3278960/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheltzer, Jason M -- Blank, Heidi M -- Pfau, Sarah J -- Tange, Yoshie -- George, Benson M -- Humpton, Timothy J -- Brito, Ilana L -- Hiraoka, Yasushi -- Niwa, Osami -- Amon, Angelika -- GM056800/GM/NIGMS NIH HHS/ -- R01 GM056800/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Aug 19;333(6045):1026-30. doi: 10.1126/science.1206412.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉David H. Koch Institute for Integrative Cancer Research and Howard Hughes Medical Institute (HHMI), Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21852501" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Chromosome Segregation ; Chromosomes, Fungal/genetics ; *DNA Damage ; *DNA Repair ; DNA Replication ; DNA, Fungal/genetics/metabolism ; *Genome, Fungal ; *Genomic Instability ; Mutagenesis ; Mutation ; Neoplasms/genetics ; Phenotype ; Rad52 DNA Repair and Recombination Protein/genetics ; *Recombination, Genetic ; Saccharomyces cerevisiae/*genetics ; Saccharomyces cerevisiae Proteins/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Activation of the yeast Hippo pathway by phosphorylation-dependent assembly of signaling complexes (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-04-13
    Description: Scaffold-assisted signaling cascades guide cellular decision-making. In budding yeast, one such signal transduction pathway called the mitotic exit network (MEN) governs the transition from mitosis to the G1 phase of the cell cycle. The MEN is conserved and in metazoans is known as the Hippo tumor-suppressor pathway. We found that signaling through the MEN kinase cascade was mediated by an unusual two-step process. The MEN kinase Cdc15 first phosphorylated the scaffold Nud1. This created a phospho-docking site on Nud1, to which the effector kinase complex Dbf2-Mob1 bound through a phosphoserine-threonine binding domain, in order to be activated by Cdc15. This mechanism of pathway activation has implications for signal transmission through other kinase cascades and might represent a general principle in scaffold-assisted signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3884217/" 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/PMC3884217/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rock, Jeremy M -- Lim, Daniel -- Stach, Lasse -- Ogrodowicz, Roksana W -- Keck, Jamie M -- Jones, Michele H -- Wong, Catherine C L -- Yates, John R 3rd -- Winey, Mark -- Smerdon, Stephen J -- Yaffe, Michael B -- Amon, Angelika -- CA112967/CA/NCI NIH HHS/ -- ES015339/ES/NIEHS NIH HHS/ -- F32 GM086038/GM/NIGMS NIH HHS/ -- GM056800/GM/NIGMS NIH HHS/ -- GM51312/GM/NIGMS NIH HHS/ -- MC_U117584228/Medical Research Council/United Kingdom -- P30 CA014051/CA/NCI NIH HHS/ -- P41 GM103533/GM/NIGMS NIH HHS/ -- P41 RR011823/RR/NCRR NIH HHS/ -- R01 ES015339/ES/NIEHS NIH HHS/ -- R01 GM051312/GM/NIGMS NIH HHS/ -- R01 GM056800/GM/NIGMS NIH HHS/ -- R29 GM056800/GM/NIGMS NIH HHS/ -- U117584228/Medical Research Council/United Kingdom -- U54 CA112967/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 May 17;340(6134):871-5. doi: 10.1126/science.1235822. Epub 2013 Apr 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23579499" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase ; Cell Cycle Proteins/chemistry/*metabolism ; Deoxyribonucleases/chemistry/*metabolism ; Enzyme Activation ; GTP-Binding Proteins/*metabolism ; *Mitosis ; Phosphoproteins/chemistry/*metabolism ; Phosphorylation ; Protein Conformation ; Protein-Serine-Threonine Kinases/*metabolism ; Saccharomyces cerevisiae/cytology/*metabolism ; Saccharomyces cerevisiae Proteins/chemistry/*metabolism ; Signal Transduction ; tRNA Methyltransferases/chemistry/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    CDC20 and CDH1: a family of substrate-specific activators of APC-dependent proteolysis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-23
    Description: Proteolysis mediated by the anaphase-promoting complex (APC) triggers chromosome segregation and exit from mitosis, yet its regulation is poorly understood. The conserved Cdc20 and Cdh1 proteins were identified as limiting, substrate-specific activators of APC-dependent proteolysis. CDC20 was required for the degradation of the APC substrate Pds1 but not for that of other APC substrates, such as Clb2 and Ase1. Conversely, cdh1Delta mutants were impaired in the degradation of Ase1 and Clb2 but not in that of Pds1. Overexpression of either CDC20 or CDH1 was sufficient to induce APC-dependent proteolysis of the appropriate target in stages of the cell cycle in which substrates are normally stable.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Visintin, R -- Prinz, S -- Amon, A -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):460-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334304" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase-Promoting Complex-Cyclosome ; Cdc20 Proteins ; Cell Cycle Proteins/genetics/*metabolism ; *Cyclin B ; Cyclins/metabolism ; Fungal Proteins/genetics/*metabolism ; G1 Phase ; Ligases/*metabolism ; Mitosis ; Mutation ; Nuclear Proteins/metabolism ; Open Reading Frames ; S Phase ; Saccharomyces cerevisiae/cytology/genetics/*metabolism ; *Saccharomyces cerevisiae Proteins ; Securin ; Substrate Specificity ; *Ubiquitin-Protein Ligase Complexes ; Ubiquitin-Protein Ligases
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Budding yeast Cdc20: a target of the spindle checkpoint (1998)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1998-03-07
    Description: The spindle checkpoint regulates the cell division cycle by keeping cells with defective spindles from leaving mitosis. In the two-hybrid system, three proteins that are components of the checkpoint, Mad1, Mad2, and Mad3, were shown to interact with Cdc20, a protein required for exit from mitosis. Mad2 and Mad3 coprecipitated with Cdc20 at all stages of the cell cycle. The binding of Mad2 depended on Mad1 and that of Mad3 on Mad1 and Mad2. Overexpression of Cdc20 allowed cells with a depolymerized spindle or damaged DNA to leave mitosis but did not overcome the arrest caused by unreplicated DNA. Mutants in Cdc20 that were resistant to the spindle checkpoint no longer bound Mad proteins, suggesting that Cdc20 is the target of the spindle checkpoint.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, L H -- Lau, L F -- Smith, D L -- Mistrot, C A -- Hardwick, K G -- Hwang, E S -- Amon, A -- Murray, A W -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):1041-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California at San Francisco, San Francisco, CA 94143-0444, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9461437" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Anaphase ; Anaphase-Promoting Complex-Cyclosome ; Cadherins ; Calcium-Binding Proteins/metabolism ; *Carrier Proteins ; Cdc20 Proteins ; Cdh1 Proteins ; Cell Cycle Proteins/chemistry/genetics/*metabolism ; DNA Damage ; DNA Replication ; Fungal Proteins/chemistry/*metabolism ; Ligases/metabolism ; Mad2 Proteins ; *Mitosis ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/metabolism ; Phosphoproteins/metabolism ; *Repressor Proteins ; Saccharomyces cerevisiae/*cytology/*metabolism ; *Saccharomyces cerevisiae Proteins ; Spindle Apparatus/*metabolism ; *Ubiquitin-Protein Ligase Complexes ; Ubiquitin-Protein Ligases
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Role of Polo-like kinase CDC5 in programming meiosis I chromosome segregation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-29
    Description: Meiosis is a specialized cell division in which two chromosome segregation phases follow a single DNA replication phase. The budding yeast Polo-like kinase Cdc5 was found to be instrumental in establishing the meiosis I chromosome segregation program. Cdc5 was required to phosphorylate and remove meiotic cohesin from chromosomes. Furthermore, in the absence of CDC5 kinetochores were bioriented during meiosis I, and Mam1, a protein essential for coorientation, failed to associate with kinetochores. Thus, sister-kinetochore coorientation and chromosome segregation during meiosis I are coupled through their dependence on CDC5.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Brian H -- Amon, Angelika -- GM62207/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 18;300(5618):482-6. Epub 2003 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, E17-233, 40 Ames Street, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12663816" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase ; Cdc20 Proteins ; Cell Cycle Proteins/metabolism ; Cell Nucleus/metabolism ; Centromere/physiology ; Chromatids/physiology ; *Chromosome Segregation ; Chromosomes, Fungal/*physiology ; Kinetochores/physiology ; *Meiosis ; Metaphase ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein Kinases/genetics/*metabolism ; Protein-Serine-Threonine Kinases ; Saccharomyces cerevisiae/enzymology/genetics/*physiology ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Securin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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