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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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7.340 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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7.340 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

Site sourced from

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

Attribution

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