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dc.contributor.authorTreister, Daniel
dc.creatorTreister, Danielen_US
dc.date.accessioned2011-10-19T18:12:13Z
dc.date.available2011-10-19T18:12:13Z
dc.date.issued2010-05
dc.identifier.citationTreister, Daniel. (2010). ATM Kinase and BLM Helicase: A Regulator and Key Player in Microhomology-Mediated End Joining (Bachelor's thesis, University of Arizona, Tucson, USA).
dc.identifier.urihttp://hdl.handle.net/10150/146020
dc.description.abstractMicrohomology-mediated end joining (MMEJ) is a class of DNA repair used to join DNA ends following a double-strand break (DSB). It represents an unfavorable and error-prone pathway because it results in deletion of nucleotides between microhomologies, as well as the deletion of one microhomology. This study utilized a DNA repair assay to measure degradation prior to end rejoining in nuclear extracts. Our results were consistent with previous studies which found that ATM plays a regulatory role in repressing nuclease degradation of DSB ends and that BLM is a required component in the MMEJ pathway. MMEJ repair products were also found to utilize GC rich microhomologies and preferred sites for rejoining. Variation among extracts from the same cell line suggest that additional trials of the repair assay must be conducted to ensure that the differences in CF, AT, and BLM nuclear extracts are the result of protein composition differences rather than variation in extract preparation.
dc.language.isoenen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.titleATM Kinase and BLM Helicase: A Regulator and Key Player in Microhomology-Mediated End Joiningen_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.levelbachelorsen_US
thesis.degree.disciplineHonors Collegeen_US
thesis.degree.disciplineBiochemistry and Molecular Biophysicsen_US
thesis.degree.nameB.S.en_US
refterms.dateFOA2018-06-28T00:00:06Z
html.description.abstractMicrohomology-mediated end joining (MMEJ) is a class of DNA repair used to join DNA ends following a double-strand break (DSB). It represents an unfavorable and error-prone pathway because it results in deletion of nucleotides between microhomologies, as well as the deletion of one microhomology. This study utilized a DNA repair assay to measure degradation prior to end rejoining in nuclear extracts. Our results were consistent with previous studies which found that ATM plays a regulatory role in repressing nuclease degradation of DSB ends and that BLM is a required component in the MMEJ pathway. MMEJ repair products were also found to utilize GC rich microhomologies and preferred sites for rejoining. Variation among extracts from the same cell line suggest that additional trials of the repair assay must be conducted to ensure that the differences in CF, AT, and BLM nuclear extracts are the result of protein composition differences rather than variation in extract preparation.


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