Endonucleases - Endodeoxyribonucleases | CU Experts | CU Boulder
Thermodynamic Interrogation of the Assembly of a Viral Genome Packaging Motor Complex
Crossover junction endodeoxyribonuclease - Wikipedia
Crossover junction endodeoxyribonucleases also play key roles in DNA repair. During cell growth and meiosis, DNA double-strand ... Crossover junction endodeoxyribonucleases with Holliday Junction resolution function have been identified in all three domains ... Crossover junction endodeoxyribonucleases catalyze Holiday junction resolution, which is the formation of separate recombinant ... Because Crossover junction endodeoxyribonucleases perform Holliday Junction resolution, a crucial step of homologous ...
Deoxyribonuclease I | Profiles RNS
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A highly sensitive selection method for directed evolution of homing endonucleases - Texas A&M University (TAMU) Scholar
Flap Endonucleases | Palmetto Profiles
PRIME PubMed | Localization of Bacillus thuringiensis Cry1A toxin-binding molecules in gypsy moth larval gut sections using...
Jacob Paiano | Harvard Catalyst Profiles | Harvard Catalyst
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In vitro resolution of poxvirus replicative intermediates into linear minichromosomes with hairpin termini by a virally induced...
Attachment of DNA to the nucleoskeleton of HeLa cells examined using physiological conditions. - Oxford Neuroscience
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Characterization of a transcription factor involved in mother cell specific transcription of the yeast HO gene. - Oxford...
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"FAN1 Removes Triplet Repeat Extrusions via a PCNA- And RFC-Dependent M" by Ashutosh S. Phadte, Mayuri Bhatia et al.
Human genome-wide association studies have identified FAN1 and several DNA mismatch repair (MMR) genes as modifiers of Huntingtons disease age of onset. In animal models, FAN1 prevents somatic expansion of CAG triplet repeats, whereas MMR proteins promote this process. To understand the molecular basis of these opposing effects, we evaluated FAN1 nuclease function on DNA extrahelical extrusions that represent key intermediates in triplet repeat expansion. Here, we describe a strand-directed, extrusion-provoked nuclease function of FAN1 that is activated by RFC, PCNA, and ATP at physiological ionic strength. Activation of FAN1 in this manner results in DNA cleavage in the vicinity of triplet repeat extrahelical extrusions thereby leading to their removal in human cell extracts. The role of PCNA and RFC is to confer strand directionality to the FAN1 nuclease, and this reaction requires a physical interaction between PCNA and FAN1. Using cell extracts, we show that FAN1-dependent CAG extrusion removal