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7.343 The Radical Consequences of Respiration: Reactive Oxygen Species in Aging and Disease (MIT) 7.343 The Radical Consequences of Respiration: Reactive Oxygen Species in Aging and Disease (MIT)

Description

This course will start with a survey of basic oxygen radical biochemistry followed by a discussion of the mechanisms of action of cellular as well as dietary antioxidants. After considering the normal physiological roles of oxidants, we will examine the effects of elevated ROS and a failure of cellular redox capacity on the rate of organismal and cellular aging as well as on the onset and progression of several major diseases that are often age-related. Topics will include ROS-induced effects on stem cell regeneration, insulin resistance, heart disease, neurodegenerative disorders, and cancer. The role of antioxidants in potential therapeutic strategies for modulating ROS levels will also be discussed. This course is one of many Advanced Undergraduate Seminars offered by the Biology D This course will start with a survey of basic oxygen radical biochemistry followed by a discussion of the mechanisms of action of cellular as well as dietary antioxidants. After considering the normal physiological roles of oxidants, we will examine the effects of elevated ROS and a failure of cellular redox capacity on the rate of organismal and cellular aging as well as on the onset and progression of several major diseases that are often age-related. Topics will include ROS-induced effects on stem cell regeneration, insulin resistance, heart disease, neurodegenerative disorders, and cancer. The role of antioxidants in potential therapeutic strategies for modulating ROS levels will also be discussed. This course is one of many Advanced Undergraduate Seminars offered by the Biology D

Subjects

reactive oxygen species | reactive oxygen species | oxygen | oxygen | ROS | ROS | energy | energy | mitochondria | mitochondria | cell signaling | cell signaling | anti-pathogen | anti-pathogen | oxidative damage | oxidative damage | oncogene | oncogene | antioxidant | antioxidant | insulin resistance | insulin resistance | diabetes | diabetes | stem cell | stem cell | neurodegenerative | neurodegenerative | ischemic | ischemic | ATP | ATP | pathways | pathways | NADPH | NADPH | nox | nox | psd | psd | programmed cell death | programmed cell death | apoptosis | apoptosis | hsc | hsc | hematopoietic | hematopoietic

License

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7.340 Ubiquitination: The Proteasome and Human Disease (MIT) 7.340 Ubiquitination: The Proteasome and Human Disease (MIT)

Description

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. This seminar provides a deeper understanding of the post-translational mechanisms evolved by eukaryotic cells to target proteins for degradation. Students learn how proteins are recognized and degraded by specific machinery (the proteasome) through their previous tagging with another small protein, ubiquitin. Additional topics include principles of ubiquitin-proteasome function, its control of the most important cellular pathways, and the implication of this system in different human diseases. Finally, spe 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. This seminar provides a deeper understanding of the post-translational mechanisms evolved by eukaryotic cells to target proteins for degradation. Students learn how proteins are recognized and degraded by specific machinery (the proteasome) through their previous tagging with another small protein, ubiquitin. Additional topics include principles of ubiquitin-proteasome function, its control of the most important cellular pathways, and the implication of this system in different human diseases. Finally, spe

Subjects

ubiquitination | ubiquitination | ubiquitin | ubiquitin | proteasome | proteasome | post-translational mechanisms | post-translational mechanisms | ubiquitin-conjugation system | ubiquitin-conjugation system | neurodegenerative diseases | neurodegenerative diseases | immune response | immune response | cell cycle regulation | cell cycle regulation | apoptosis | apoptosis | signal transduction pathways | signal transduction pathways | tumorigenesis | tumorigenesis | protein degradation | protein degradation | Endoplasmic Reticulum Associated Degradation Pathway | Endoplasmic Reticulum Associated Degradation Pathway | ligases | ligases | translocated proteins | translocated proteins | misfolded proteins | misfolded proteins | trafficking membranes | trafficking membranes | cell cycle control | cell cycle control | programmed cell death | programmed cell death | Huntington's Disease | Huntington's Disease | Von Hippel-Lindau Disease | Von Hippel-Lindau Disease

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.342 Cancer Biology: From Basic Research to the Clinic (MIT) 7.342 Cancer Biology: From Basic Research to the Clinic (MIT)

Description

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. In 1971, President Nixon declared the "War on Cancer," but after three decades the war is still raging. How much progress have we made toward winning the war and what are we doing to improve the fight? Understanding the molecular and cellular events involved in tumor formation, progression, and metastasis is crucial to the development of innovative therapy for cancer patients. Insights into these processes have been gleaned through basic research using biochemical, molecular, and genetic ana 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. In 1971, President Nixon declared the "War on Cancer," but after three decades the war is still raging. How much progress have we made toward winning the war and what are we doing to improve the fight? Understanding the molecular and cellular events involved in tumor formation, progression, and metastasis is crucial to the development of innovative therapy for cancer patients. Insights into these processes have been gleaned through basic research using biochemical, molecular, and genetic ana

Subjects

cancer | cancer | tumor | tumor | metastasis | metastasis | genetic analysis | genetic analysis | cancer biology | cancer biology | model organisms | model organisms | genetic pathways | genetic pathways | uncontrolled growth | uncontrolled growth | tumor suppressor genes | tumor suppressor genes | oncogenes | oncogenes | tumor initiation | tumor initiation | cell cycle | cell cycle | chromosomal aberration | chromosomal aberration | apoptosis | apoptosis | cell death | cell death | signal transduction pathways | signal transduction pathways | proto-oncogene | proto-oncogene | mutation | mutation | DNA mismatch repair | DNA mismatch repair | telomeres | telomeres | mouse models | mouse models | tissue specificity | tissue specificity | malignancy | malignancy | stem cells | stem cells | therapeutic resistance | therapeutic resistance | differentiation | differentiation | caner research | caner research | cancer therapeutics | cancer therapeutics | chemotherapy | chemotherapy

License

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7.340 Immune Evasion: How Sneaky Pathogens Avoid Host Surveillance (MIT) 7.340 Immune Evasion: How Sneaky Pathogens Avoid Host Surveillance (MIT)

Description

Every infection consists of a battle between the invading pathogen and the resisting host. To be successful, a pathogen must escape the many defenses of the host immune system until it can replicate and spread to another host. A pathogen must prevent one of three stages of immune function: detection, activation, or effector function. Examples of disease-specific immune evasion and the mechanisms used by pathogens to prevail over their hosts' immune systems are discussed. Also considered is what these host-pathogen interactions reveal about the normal function of the immune system and basic cell biological processes, such as protein maturation and degradation. Every infection consists of a battle between the invading pathogen and the resisting host. To be successful, a pathogen must escape the many defenses of the host immune system until it can replicate and spread to another host. A pathogen must prevent one of three stages of immune function: detection, activation, or effector function. Examples of disease-specific immune evasion and the mechanisms used by pathogens to prevail over their hosts' immune systems are discussed. Also considered is what these host-pathogen interactions reveal about the normal function of the immune system and basic cell biological processes, such as protein maturation and degradation.

Subjects

immunology | immunology | immune system | immune system | immune evasion | immune evasion | pathogen | pathogen | effector function | effector function | infections | infections | Human cytomegalovirus | Human cytomegalovirus | Human Immunodeficiency Virus | Human Immunodeficiency Virus | CD4 cells | CD4 cells | CD8 cells | CD8 cells | T cells | T cells | surace receptors | surace receptors | cell lysis | cell lysis | host-pathogen interactions | host-pathogen interactions | host surveillance | host surveillance | antibodies | antibodies | MHC class I | MHC class I | blood-borne pathogens | blood-borne pathogens | macrophages | macrophages | phagocytosis | phagocytosis | endocytosis | endocytosis | degradation | degradation | antigen | antigen | apoptosis | apoptosis | cytokines | cytokines | immune response | immune response

License

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7.341 DNA Damage Checkpoints: The Emergency Brake on the Road to Cancer (MIT) 7.341 DNA Damage Checkpoints: The Emergency Brake on the Road to Cancer (MIT)

Description

The DNA contained in human cells is under constant attack by both exogenous and endogenous agents that can damage one of its three billion base pairs. To cope with this permanent exposure to DNA-damaging agents, such as the sun's radiation or by-products of our normal metabolism, powerful DNA damage checkpoints have evolved that allow organisms to survive this constant assault on their genomes. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understanding of checkpoints that act as powerful emergency brakes to prevent cancer. We will consider basic principles of cell proliferation and molecular details of the DNA damage response. We will discuss the methods and model organisms typically used in this field as well as how an The DNA contained in human cells is under constant attack by both exogenous and endogenous agents that can damage one of its three billion base pairs. To cope with this permanent exposure to DNA-damaging agents, such as the sun's radiation or by-products of our normal metabolism, powerful DNA damage checkpoints have evolved that allow organisms to survive this constant assault on their genomes. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understanding of checkpoints that act as powerful emergency brakes to prevent cancer. We will consider basic principles of cell proliferation and molecular details of the DNA damage response. We will discuss the methods and model organisms typically used in this field as well as how an

Subjects

DNA | DNA | damage checkpoints | damage checkpoints | cancer | cancer | cells | cells | human cells | human cells | exogenous | exogenous | endogenous | endogenous | checkpoints | checkpoints | gene | gene | signaling | signaling | cancer biology | cancer biology | cancer prevention | cancer prevention | primary sources | primary sources | discussion | discussion | DNA damage | DNA damage | molecular | molecular | enzyme | enzyme | cell cycle | cell cycle | extracellular cues | extracellular cues | growth factors | growth factors | Cdk regulation | Cdk regulation | cyclin-dependent kinase | cyclin-dependent kinase | p53 | p53 | tumor suppressor | tumor suppressor | apoptosis | apoptosis | MDC1 | MDC1 | H2AX | H2AX | Rad50 | Rad50 | Fluorescence activated cell sorter | Fluorescence activated cell sorter | Chk1 | Chk1 | mutant | mutant

License

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7.344 Tumor Suppressor Gene p53: How the Guardian of our Genome Prevents Cancer (MIT) 7.344 Tumor Suppressor Gene p53: How the Guardian of our Genome Prevents Cancer (MIT)

Description

Cancer is a leading cause of death worldwide. Cancer involves uncontrolled cell growth, resistance to cell death, failure to differentiate into a particular cell type, and increased cellular motility. A family of gate-keeper genes, known as tumor suppressor genes, plays important roles in preventing the initiation and progression of cancer. Among these, p53 is the most famous. Because of its essential role in maintaining genomic integrity, p53 is often called the guardian of the genome. During this course, we will study how p53 serves as a pivotal tumor suppressor gene in preventing cancer.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 disc Cancer is a leading cause of death worldwide. Cancer involves uncontrolled cell growth, resistance to cell death, failure to differentiate into a particular cell type, and increased cellular motility. A family of gate-keeper genes, known as tumor suppressor genes, plays important roles in preventing the initiation and progression of cancer. Among these, p53 is the most famous. Because of its essential role in maintaining genomic integrity, p53 is often called the guardian of the genome. During this course, we will study how p53 serves as a pivotal tumor suppressor gene in preventing cancer.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 disc

Subjects

tumor suppressor gene | tumor suppressor gene | p53 | p53 | p53 protein | p53 protein | cancer | cancer | cell-growth signals | cell-growth signals | cell cycle regulation | cell cycle regulation | DNA damage | DNA damage | DNA repair | DNA repair | programmed cell death | programmed cell death | apoptosis | apoptosis | genome integrity | genome integrity | oncogenes | oncogenes | p53 mutations | p53 mutations | mouse cancer models | mouse cancer models | Mdm2 | Mdm2 | microRNA | microRNA

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.343 When Development Goes Awry: How Cancer Co-opts Mechanisms of Embryogensis (MIT) 7.343 When Development Goes Awry: How Cancer Co-opts Mechanisms of Embryogensis (MIT)

Description

During this course, we will study the similarities between cancer and normal development to understand how tumors co-opt normal developmental processes to facilitate cancer initiation, maintenance and progression. We will examine critical signaling pathways that govern these processes and, importantly, how some of these pathways hold promise as therapeutic targets for cancer treatment. We will discuss how future treatments might be personalized to target cancer cells in specific patients. We will also consider examples of newly-approved drugs that have dramatically helped patients combat this devastating disease. 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 res During this course, we will study the similarities between cancer and normal development to understand how tumors co-opt normal developmental processes to facilitate cancer initiation, maintenance and progression. We will examine critical signaling pathways that govern these processes and, importantly, how some of these pathways hold promise as therapeutic targets for cancer treatment. We will discuss how future treatments might be personalized to target cancer cells in specific patients. We will also consider examples of newly-approved drugs that have dramatically helped patients combat this devastating disease. 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 res

Subjects

cancer | cancer | embryogenesis | embryogenesis | sonic hedgehog | sonic hedgehog | tumor | tumor | signaling | signaling | proto-oncogene | proto-oncogene | Kras | Kras | apoptosis | apoptosis | self-renewal | self-renewal | regeneration | regeneration | angiogenesis | angiogenesis | VEGF | VEGF | tumorigenesis | tumorigenesis | metastasis | metastasis | microRNA | microRNA

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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7.341 The DNA Damage Response as a Target for Anti-Cancer Therapy (MIT) 7.341 The DNA Damage Response as a Target for Anti-Cancer Therapy (MIT)

Description

Cellular responses to DNA damage constitute one of the most important fields in cancer biology. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understand of cell cycle regulation and DNA damage checkpoints that act as powerful emergency brakes to prevent cancer. 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. Cellular responses to DNA damage constitute one of the most important fields in cancer biology. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understand of cell cycle regulation and DNA damage checkpoints that act as powerful emergency brakes to prevent cancer. 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.

Subjects

DNA | DNA | damage checkpoints | damage checkpoints | cancer | cancer | cells | cells | human cells | human cells | exogenous | exogenous | endogenous | endogenous | checkpoints | checkpoints | gene | gene | signaling | signaling | cancer biology | cancer biology | cancer prevention | cancer prevention | primary sources | primary sources | discussion | discussion | DNA damage | DNA damage | molecular | molecular | enzyme | enzyme | cell cycle | cell cycle | extracellular cues | extracellular cues | growth factors | growth factors | Cdk regulation | Cdk regulation | cyclin-dependent kinase | cyclin-dependent kinase | p53 | p53 | tumor suppressor | tumor suppressor | apoptosis | apoptosis | MDC1 | MDC1 | H2AX | H2AX | Rad50 | Rad50 | Fluorescence activated cell sorter | Fluorescence activated cell sorter | Chk1 | Chk1 | mutant | mutant

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see http://ocw.mit.edu/terms/index.htm

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Apoptosis and Cancer

Description

The contents are free to adopt or adapt under the Creative Commons License for non-commercial use. If you are repurposing this resource for your own teaching, please deposit the updated version on JorumOpen and/or email the links to the author at bssmvh@bath.ac.uk

Subjects

apoptosis | bioukoer | caspases | Biological sciences | C000

License

Attribution-Noncommercial-Share Alike 2.0 UK: England & Wales Attribution-Noncommercial-Share Alike 2.0 UK: England & Wales http://creativecommons.org/licenses/by-nc-sa/2.0/uk/ http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

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7.340 Ubiquitination: The Proteasome and Human Disease (MIT)

Description

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. This seminar provides a deeper understanding of the post-translational mechanisms evolved by eukaryotic cells to target proteins for degradation. Students learn how proteins are recognized and degraded by specific machinery (the proteasome) through their previous tagging with another small protein, ubiquitin. Additional topics include principles of ubiquitin-proteasome function, its control of the most important cellular pathways, and the implication of this system in different human diseases. Finally, spe

Subjects

ubiquitination | ubiquitin | proteasome | post-translational mechanisms | ubiquitin-conjugation system | neurodegenerative diseases | immune response | cell cycle regulation | apoptosis | signal transduction pathways | tumorigenesis | protein degradation | Endoplasmic Reticulum Associated Degradation Pathway | ligases | translocated proteins | misfolded proteins | trafficking membranes | cell cycle control | programmed cell death | Huntington's Disease | Von Hippel-Lindau Disease

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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7.341 DNA Damage Checkpoints: The Emergency Brake on the Road to Cancer (MIT)

Description

The DNA contained in human cells is under constant attack by both exogenous and endogenous agents that can damage one of its three billion base pairs. To cope with this permanent exposure to DNA-damaging agents, such as the sun's radiation or by-products of our normal metabolism, powerful DNA damage checkpoints have evolved that allow organisms to survive this constant assault on their genomes. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understanding of checkpoints that act as powerful emergency brakes to prevent cancer. We will consider basic principles of cell proliferation and molecular details of the DNA damage response. We will discuss the methods and model organisms typically used in this field as well as how an

Subjects

DNA | damage checkpoints | cancer | cells | human cells | exogenous | endogenous | checkpoints | gene | signaling | cancer biology | cancer prevention | primary sources | discussion | DNA damage | molecular | enzyme | cell cycle | extracellular cues | growth factors | Cdk regulation | cyclin-dependent kinase | p53 | tumor suppressor | apoptosis | MDC1 | H2AX | Rad50 | Fluorescence activated cell sorter | Chk1 | mutant

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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The making of individual differences

Description

How do we become individuals? This unit looks at how genes and the environment interact making each of us unique. Looking at the period between conception and birth you will examine the issues of nature or nurture to see which has the greatest impact.

Subjects

science and nature | apoptosis | behaviour | brain | development | environment | genetics | nervous system | neurotrophins | phenotype | plasticity | sensitive_period | transcription | Education | X000

License

Attribution-Noncommercial-Share Alike 2.0 UK: England & Wales Attribution-Noncommercial-Share Alike 2.0 UK: England & Wales http://creativecommons.org/licenses/by-nc-sa/2.0/uk/ http://creativecommons.org/licenses/by-nc-sa/2.0/uk/

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7.344 Tumor Suppressor Gene p53: How the Guardian of our Genome Prevents Cancer (MIT)

Description

Cancer is a leading cause of death worldwide. Cancer involves uncontrolled cell growth, resistance to cell death, failure to differentiate into a particular cell type, and increased cellular motility. A family of gate-keeper genes, known as tumor suppressor genes, plays important roles in preventing the initiation and progression of cancer. Among these, p53 is the most famous. Because of its essential role in maintaining genomic integrity, p53 is often called the guardian of the genome. During this course, we will study how p53 serves as a pivotal tumor suppressor gene in preventing cancer.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 disc

Subjects

tumor suppressor gene | p53 | p53 protein | cancer | cell-growth signals | cell cycle regulation | DNA damage | DNA repair | programmed cell death | apoptosis | genome integrity | oncogenes | p53 mutations | mouse cancer models | Mdm2 | microRNA

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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7.343 When Development Goes Awry: How Cancer Co-opts Mechanisms of Embryogensis (MIT)

Description

During this course, we will study the similarities between cancer and normal development to understand how tumors co-opt normal developmental processes to facilitate cancer initiation, maintenance and progression. We will examine critical signaling pathways that govern these processes and, importantly, how some of these pathways hold promise as therapeutic targets for cancer treatment. We will discuss how future treatments might be personalized to target cancer cells in specific patients. We will also consider examples of newly-approved drugs that have dramatically helped patients combat this devastating disease. 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 res

Subjects

cancer | embryogenesis | sonic hedgehog | tumor | signaling | proto-oncogene | Kras | apoptosis | self-renewal | regeneration | angiogenesis | VEGF | tumorigenesis | metastasis | microRNA

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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7.341 The DNA Damage Response as a Target for Anti-Cancer Therapy (MIT)

Description

Cellular responses to DNA damage constitute one of the most important fields in cancer biology. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understand of cell cycle regulation and DNA damage checkpoints that act as powerful emergency brakes to prevent cancer. 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.

Subjects

DNA | damage checkpoints | cancer | cells | human cells | exogenous | endogenous | checkpoints | gene | signaling | cancer biology | cancer prevention | primary sources | discussion | DNA damage | molecular | enzyme | cell cycle | extracellular cues | growth factors | Cdk regulation | cyclin-dependent kinase | p53 | tumor suppressor | apoptosis | MDC1 | H2AX | Rad50 | Fluorescence activated cell sorter | Chk1 | mutant

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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7.343 The Radical Consequences of Respiration: Reactive Oxygen Species in Aging and Disease (MIT)

Description

This course will start with a survey of basic oxygen radical biochemistry followed by a discussion of the mechanisms of action of cellular as well as dietary antioxidants. After considering the normal physiological roles of oxidants, we will examine the effects of elevated ROS and a failure of cellular redox capacity on the rate of organismal and cellular aging as well as on the onset and progression of several major diseases that are often age-related. Topics will include ROS-induced effects on stem cell regeneration, insulin resistance, heart disease, neurodegenerative disorders, and cancer. The role of antioxidants in potential therapeutic strategies for modulating ROS levels will also be discussed. This course is one of many Advanced Undergraduate Seminars offered by the Biology D

Subjects

reactive oxygen species | oxygen | ROS | energy | mitochondria | cell signaling | anti-pathogen | oxidative damage | oncogene | antioxidant | insulin resistance | diabetes | stem cell | neurodegenerative | ischemic | ATP | pathways | NADPH | nox | psd | programmed cell death | apoptosis | hsc | hematopoietic

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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7.340 Ubiquitination: The Proteasome and Human Disease (MIT)

Description

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. This seminar provides a deeper understanding of the post-translational mechanisms evolved by eukaryotic cells to target proteins for degradation. Students learn how proteins are recognized and degraded by specific machinery (the proteasome) through their previous tagging with another small protein, ubiquitin. Additional topics include principles of ubiquitin-proteasome function, its control of the most important cellular pathways, and the implication of this system in different human diseases. Finally, spe

Subjects

ubiquitination | ubiquitin | proteasome | post-translational mechanisms | ubiquitin-conjugation system | neurodegenerative diseases | immune response | cell cycle regulation | apoptosis | signal transduction pathways | tumorigenesis | protein degradation | Endoplasmic Reticulum Associated Degradation Pathway | ligases | translocated proteins | misfolded proteins | trafficking membranes | cell cycle control | programmed cell death | Huntington's Disease | Von Hippel-Lindau Disease

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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7.342 Cancer Biology: From Basic Research to the Clinic (MIT)

Description

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. In 1971, President Nixon declared the "War on Cancer," but after three decades the war is still raging. How much progress have we made toward winning the war and what are we doing to improve the fight? Understanding the molecular and cellular events involved in tumor formation, progression, and metastasis is crucial to the development of innovative therapy for cancer patients. Insights into these processes have been gleaned through basic research using biochemical, molecular, and genetic ana

Subjects

cancer | tumor | metastasis | genetic analysis | cancer biology | model organisms | genetic pathways | uncontrolled growth | tumor suppressor genes | oncogenes | tumor initiation | cell cycle | chromosomal aberration | apoptosis | cell death | signal transduction pathways | proto-oncogene | mutation | DNA mismatch repair | telomeres | mouse models | tissue specificity | malignancy | stem cells | therapeutic resistance | differentiation | caner research | cancer therapeutics | chemotherapy

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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7.340 Immune Evasion: How Sneaky Pathogens Avoid Host Surveillance (MIT)

Description

Every infection consists of a battle between the invading pathogen and the resisting host. To be successful, a pathogen must escape the many defenses of the host immune system until it can replicate and spread to another host. A pathogen must prevent one of three stages of immune function: detection, activation, or effector function. Examples of disease-specific immune evasion and the mechanisms used by pathogens to prevail over their hosts' immune systems are discussed. Also considered is what these host-pathogen interactions reveal about the normal function of the immune system and basic cell biological processes, such as protein maturation and degradation.

Subjects

immunology | immune system | immune evasion | pathogen | effector function | infections | Human cytomegalovirus | Human Immunodeficiency Virus | CD4 cells | CD8 cells | T cells | surace receptors | cell lysis | host-pathogen interactions | host surveillance | antibodies | MHC class I | blood-borne pathogens | macrophages | phagocytosis | endocytosis | degradation | antigen | apoptosis | cytokines | immune response

License

Content within individual OCW courses is (c) by the individual authors unless otherwise noted. MIT OpenCourseWare materials are licensed by the Massachusetts Institute of Technology under a Creative Commons License (Attribution-NonCommercial-ShareAlike). For further information see https://ocw.mit.edu/terms/index.htm

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Cancer Biology

Description

This course will cover the origins of cancer and the genetic and cellular basis for cancer. It will examine the factors that have been implicated in triggering cancers, the intercellular interactions involved in cancer proliferation, current treatments for cancer and how these are designed, and future research and treatment directions for cancer therapy. This free course may be completed online at any time. See course site for detailed overview and learning outcomes. (Biology 404)

Subjects

biology | cancer | genes | death | carcinogens | expression | regulation | inhibitors | apoptosis | immortality | therapy | prevention | Biological sciences | C000

License

Attribution 2.0 UK: England & Wales Attribution 2.0 UK: England & Wales http://creativecommons.org/licenses/by/2.0/uk/ http://creativecommons.org/licenses/by/2.0/uk/

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