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7.16 Experimental Molecular Biology: Biotechnology II (MIT) 7.16 Experimental Molecular Biology: Biotechnology II (MIT)

Description

The course applies molecular biology and reverse genetics approaches to the study of apoptosis, or programmed cell death (PCD), in Drosophila cells. RNA interference (RNAi), or double stranded RNA-mediated gene silencing, will be used to inhibit expression of candidate apoptosis-related genes in cultured Drosophila cells. Teams of 2 or 3 students will design and carry out experiments to address questions about the genes involved in the regulation and execution of PCD in this system. Some projects involve the use of DNA damaging agents or other cytotoxic chemicals or drugs to help understand the pathways that control a cell's decision to undergo apoptosis. Instruction and practice in written and oral communication are provided. The course applies molecular biology and reverse genetics approaches to the study of apoptosis, or programmed cell death (PCD), in Drosophila cells. RNA interference (RNAi), or double stranded RNA-mediated gene silencing, will be used to inhibit expression of candidate apoptosis-related genes in cultured Drosophila cells. Teams of 2 or 3 students will design and carry out experiments to address questions about the genes involved in the regulation and execution of PCD in this system. Some projects involve the use of DNA damaging agents or other cytotoxic chemicals or drugs to help understand the pathways that control a cell's decision to undergo apoptosis. Instruction and practice in written and oral communication are provided.

Subjects

RNAi | RNAi | RNA interference | RNA interference | programmed cell death | programmed cell death | Drosophilia | Drosophilia | PCD | PCD | mRNA | mRNA | lab notebook | lab notebook | scientific writing | scientific writing | RT-PCR | RT-PCR | S2 RNA | S2 RNA | S2 | S2 | cell culture | cell culture | genetic transcription | genetic transcription | dsRNA | dsRNA | bioinformatics | bioinformatics

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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7.344 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 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

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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7.340 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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7.340 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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7.344 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 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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7.16 Experimental Molecular Biology: Biotechnology II (MIT)

Description

The course applies molecular biology and reverse genetics approaches to the study of apoptosis, or programmed cell death (PCD), in Drosophila cells. RNA interference (RNAi), or double stranded RNA-mediated gene silencing, will be used to inhibit expression of candidate apoptosis-related genes in cultured Drosophila cells. Teams of 2 or 3 students will design and carry out experiments to address questions about the genes involved in the regulation and execution of PCD in this system. Some projects involve the use of DNA damaging agents or other cytotoxic chemicals or drugs to help understand the pathways that control a cell's decision to undergo apoptosis. Instruction and practice in written and oral communication are provided.

Subjects

RNAi | RNA interference | programmed cell death | Drosophilia | PCD | mRNA | lab notebook | scientific writing | RT-PCR | S2 RNA | S2 | cell culture | genetic transcription | dsRNA | bioinformatics

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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https://ocw.mit.edu/rss/all/mit-allcourses.xml

Attribution

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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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