Rtt
Mostrando 25-34 de 34 artigos, teses e dissertações.
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25. DNA polymerase ɛ, acetylases and remodellers cooperate to form a specialized chromatin structure at a tRNA insulator
Insulators bind transcription factors and use chromatin remodellers and modifiers to mediate insulation. In this report, we identified proteins required for the efficient formation and maintenance of a specialized chromatin structure at the yeast tRNA insulator. The histone acetylases, SAS-I and NuA4, functioned in insulation, independently of tRNA and did n
Nature Publishing Group.
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26. Expression of MeCP2 in postmitotic neurons rescues Rett syndrome in mice
Mutations in MECP2 are the cause of Rett syndrome (RTT) in humans, a neurodevelopmental disorder that affects mainly girls. MeCP2 is a protein that binds CpG dinucleotides and is thought to act as a global transcriptional repressor. It is highly expressed in neurons, but not in glia, of the postnatal brain. The timing of MeCP2 activation correlates with the
National Academy of Sciences.
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27. Torpedo Nuclease Rat1 Is Insufficient to Terminate RNA Polymerase II in Vitro*
Termination of RNA polymerase (pol) II transcription in vivo requires the 5′-RNA exonuclease Rat1. It was proposed that Rat1 degrades RNA from the 5′-end that is created by transcript cleavage, catches up with elongating pol II, and acts like a Torpedo that removes pol II from DNA. Here we test the Torpedo model in an in vitro system based on bead-couple
American Society for Biochemistry and Molecular Biology.
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28. Clinical Emergence of Entecavir-Resistant Hepatitis B Virus Requires Additional Substitutions in Virus Already Resistant to Lamivudine
Entecavir (ETV) exhibits potent antiviral activity in patients chronically infected with wild-type or lamivudine (3TC)-resistant (3TCr) hepatitis B virus (HBV). Among the patients treated in phase II ETV clinical trials, two patients for whom previous therapies had failed exhibited virologic breakthrough while on ETV. Isolates from these patients (arbitraril
American Society for Microbiology.
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29. Reduced cortical activity due to a shift in the balance between excitation and inhibition in a mouse model of Rett Syndrome
Rett Syndrome (RTT) is a devastating neurological disorder that is caused by mutations in the MECP2 gene. Mecp2-mutant mice have been used as a model system to study the disease mechanism. Our previous work has suggested that MeCP2 malfunction in neurons is the primary cause of RTT in the mouse. However, the neurophysiological consequences of MeCP2 malfuncti
National Academy of Sciences.
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30. Temporal and regional differences in the olfactory proteome as a consequence of MeCP2 deficiency
Rett syndrome (RTT) is a neurodevelopmental disorder caused by mutations in the gene encoding MeCP2. By binding to methylated CpG dinucleotide promoter regions, MeCP2 acts as a transcriptional repressor, predicting that its absence might result in widespread aberrant gene transcription, leading to the RTT phenotype. Considering this potentially broad action
National Academy of Sciences.
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31. Mms22p protects Saccharomyces cerevisiae from DNA damage induced by topoisomerase II
The cleavage reaction of topoisomerase II, which creates double-stranded DNA breaks, plays a central role in both the cure and initiation of cancer. Therefore, it is important to understand the cellular processes that repair topoisomerase II-generated DNA damage. Using a genome-wide approach with Saccharomyces cerevisiae, we found that Δmre11, Δxrs2, Δrad
Oxford University Press.
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32. Posttranslational Regulation of Ty1 Retrotransposition by Mitogen-Activated Protein Kinase Fus3
Ty1 retrotransposons in Saccharomyces cerevisiae are maintained in a state of transpositional dormancy. We isolated a mutation, rtt100-1, that increases the transposition of genomic Ty1 elements 18- to 56-fold but has little effect on the transposition of related Ty2 elements. rtt100-1 was shown to be a null allele of the FUS3 gene, which encodes a haploid-s
American Society for Microbiology.
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33. Nucleotide Excision Repair/TFIIH Helicases Rad3 and Ssl2 Inhibit Short-Sequence Recombination and Ty1 Retrotransposition by Similar Mechanisms
Eukaryotic genomes contain potentially unstable sequences whose rearrangement threatens genome structure and function. Here we show that certain mutant alleles of the nucleotide excision repair (NER)/TFIIH helicase genes RAD3 and SSL2 (RAD25) confer synthetic lethality and destabilize the Saccharomyces cerevisiae genome by increasing both short-sequence reco
American Society for Microbiology.
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34. The ctf13-30/CTF13 Genomic Haploinsufficiency Modifier Screen Identifies the Yeast Chromatin Remodeling Complex RSC, Which Is Required for the Establishment of Sister Chromatid Cohesion
The budding yeast centromere-kinetochore complex ensures high-fidelity chromosome segregation in mitosis and meiosis by mediating the attachment and movement of chromosomes along spindle microtubules. To identify new genes and pathways whose function impinges on chromosome transmission, we developed a genomic haploinsufficiency modifier screen and used ctf13
American Society for Microbiology.