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dc.contributor.authorFerullo, Daniel
dc.coverage.temporalSpring 2011
dc.date.accessioned2023-03-06T17:19:18Z
dc.date.available2023-03-06T17:19:18Z
dc.date.issued2011-06
dc.identifier7.342-Spring2011
dc.identifier.other7.342
dc.identifier.otherIMSCP-MD5-e1d922e75bfd87e8f03d812d05066f34
dc.identifier.urihttps://hdl.handle.net/1721.1/148349
dc.description.abstractThe primary role of mitochondria is to produce 90% of a cell's energy in the form of ATP through a process called oxidative phosphorylation. A variety of clinical disorders have been shown to include "mitochondrial dysfunction," which loosely refers to defective oxidative phosphorylation and usually coincides with the occurrence of excess Reactive Oxygen Species (ROS) production, placing cells under oxidative stress. A known cause and effect of oxidative stress is damage to and mutation of mitochondrial DNA. We will use this class to explore issues relating to mitochondrial DNA integrity and how it can be damaged, repaired, mutated, and compromised in human diseases. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. Many instructors of the Advanced Undergraduate Seminars are postdoctoral scientists with a strong interest in teaching.en
dc.language.isoen-US
dc.rightsThis site (c) Massachusetts Institute of Technology 2023. Content within individual courses is (c) by the individual authors unless otherwise noted. The Massachusetts Institute of Technology is providing this Work (as defined below) under the terms of this Creative Commons public license ("CCPL" or "license") unless otherwise noted. The Work is protected by copyright and/or other applicable law. Any use of the work other than as authorized under this license is prohibited. By exercising any of the rights to the Work provided here, You (as defined below) accept and agree to be bound by the terms of this license. The Licensor, the Massachusetts Institute of Technology, grants You the rights contained here in consideration of Your acceptance of such terms and conditions.en
dc.rightsAttribution-NonCommercial-ShareAlike 3.0 Unported*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/*
dc.subjectmitochondriaen
dc.subjecthuman diseaseen
dc.subjectATPen
dc.subjectoxidative phosphorylationen
dc.subjectmitochondrial genomeen
dc.subjectReactive Oxygen Species (ROS)en
dc.subjectmitochondrial dysfunctionen
dc.subjectoxidative stress, 8-oxoguanineen
dc.subject8-oxoGen
dc.subjectmtDNAen
dc.subjectOgg1en
dc.subjectOxoguanine glycosylaseen
dc.subjectmitochondrial DNA polymeraseen
dc.subjectAlzheimer’s diseaseen
dc.subjectParkinson’s diseaseen
dc.subjectY955Cen
dc.subjectMitochondrial DNA depletion syndromesen
dc.title7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases, Spring 2011en
dc.title.alternativePowerhouse Rules: The Role of Mitochondria in Human Diseasesen
dc.typeLearning Object
dc.typeLearning Object
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biology
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biology
dc.audience.educationlevelUndergraduate
dc.subject.cip511010en
dc.date.updated2023-03-06T17:19:24Z


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