7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases, Spring 2011

The 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 phos...

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Main Author: Ferullo, Daniel
Other Authors: Massachusetts Institute of Technology. Department of Biology
Format: Learning Object
Language:en-US
Published: 2023
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Online Access:https://hdl.handle.net/1721.1/148349
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author Ferullo, Daniel
author2 Massachusetts Institute of Technology. Department of Biology
author_facet Massachusetts Institute of Technology. Department of Biology
Ferullo, Daniel
author_sort Ferullo, Daniel
collection MIT
description The 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.
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spelling mit-1721.1/1483492025-02-26T22:05:47Z 7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases, Spring 2011 Powerhouse Rules: The Role of Mitochondria in Human Diseases Ferullo, Daniel Massachusetts Institute of Technology. Department of Biology Massachusetts Institute of Technology. Department of Biology mitochondria human disease ATP oxidative phosphorylation mitochondrial genome Reactive Oxygen Species (ROS) mitochondrial dysfunction oxidative stress, 8-oxoguanine 8-oxoG mtDNA Ogg1 Oxoguanine glycosylase mitochondrial DNA polymerase Alzheimer’s disease Parkinson’s disease Y955C Mitochondrial DNA depletion syndromes 511010 The 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. 2023-03-06T17:19:18Z 2023-03-06T17:19:18Z 2011-06 2023-03-06T17:19:24Z Learning Object Learning Object 7.342-Spring2011 7.342 IMSCP-MD5-e1d922e75bfd87e8f03d812d05066f34 https://hdl.handle.net/1721.1/148349 en-US This 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. 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spellingShingle mitochondria
human disease
ATP
oxidative phosphorylation
mitochondrial genome
Reactive Oxygen Species (ROS)
mitochondrial dysfunction
oxidative stress, 8-oxoguanine
8-oxoG
mtDNA
Ogg1
Oxoguanine glycosylase
mitochondrial DNA polymerase
Alzheimer’s disease
Parkinson’s disease
Y955C
Mitochondrial DNA depletion syndromes
511010
Ferullo, Daniel
7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases, Spring 2011
title 7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases, Spring 2011
title_full 7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases, Spring 2011
title_fullStr 7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases, Spring 2011
title_full_unstemmed 7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases, Spring 2011
title_short 7.342 Powerhouse Rules: The Role of Mitochondria in Human Diseases, Spring 2011
title_sort 7 342 powerhouse rules the role of mitochondria in human diseases spring 2011
topic mitochondria
human disease
ATP
oxidative phosphorylation
mitochondrial genome
Reactive Oxygen Species (ROS)
mitochondrial dysfunction
oxidative stress, 8-oxoguanine
8-oxoG
mtDNA
Ogg1
Oxoguanine glycosylase
mitochondrial DNA polymerase
Alzheimer’s disease
Parkinson’s disease
Y955C
Mitochondrial DNA depletion syndromes
511010
url https://hdl.handle.net/1721.1/148349
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