VO 7 cell biology

• Lecture 1: The cell and its components
• Lecture 2: The cell and its components II; Analysing Cells, Molecules and Systems
• Lecture 3: Membrane structure and function
• Lecture 4: Cytoskeleton and Cell Migration
• Understanding senescence is important for medical research.
• Senescence is observed in age-related diseases.
• Oncogene-induced senescence is a type of cellular senescence.
• Senescence protects against cancer.
• Replicative senescence is a type of cellular senescence.
• Lecture 7: Cell death and cell senescence
• Cells from older people undergo fewer divisions than cells from younger people, suggesting that the total number of divisions since birth is important.
• Telomeres shorten with each cell division, and cellular senescence is triggered when cells acquire critically short telomeres.
• Each round of DNA replication leaves 50-200 bp DNA unreplicated at the 3' end.
• Replicative senescence: Cells stop dividing after around 40-50 divisions.
• Lecture 5: Cell cycle
• Lecture 6: Chromosome segregation and cell division
• The extrinsic pathway of apoptosis is activated by cell-surface death receptors.
• Cellular senescence is discussed in Chapter 5 of the book "Senescence" by McHugh and Gil.
• Apoptosis is a programmed cell death process that eliminates unwanted cells.
• Caspases mediate the intrinsic proteolytic cascade in apoptosis.
• The intrinsic pathway of apoptosis depends on mitochondria.
• Bcl2 proteins regulate the intrinsic pathway of apoptosis by governing mitochondrial outer membrane permeabilization.
• Normal development requires apoptosis, such as the separation of fingers and toes in a developing human embryo.
• Defective apoptotic processes have been implicated in a variety of diseases, including cancer and atrophy.
• Apoptotic cells are morphologically and biochemically recognizable, with broken DNA and characteristic cell changes.
• The immune system relies on apoptosis.
• Up to 100 billion cells die each day due to apoptosis in the average human adult.
• Apoptosis is programmed cell death that confers advantages during an organism's lifecycle.
• Apoptosis eliminates genetically unstable cells.
• Cellular senescence can be triggered by stress-induced factors.
• Senescent cells undergo morphological changes, such as becoming flat, large, vacuolized, and occasionally multinucleate.
• Cellular senescence is a cellular program that induces a stable growth arrest accompanied by distinct phenotypic alterations.
• Senescent cells are not dead and remain metabolically active.
• Senescent cells also undergo chromatin remodelling, metabolic reprogramming, increased autophagy, and the implementation of a complex pro-inflammatory secretome.
• Replicative senescence occurs when fibroblast cultures derived from human skin divide a certain number of times and then stop dividing.
• Caspases are cysteine proteases that cleave substrates at specific aspartic acids.
• Apoptosis depends on an intrinsic proteolytic cascade mediated by caspases.
• Cell-surface death receptors activate the extrinsic pathway of apoptosis.
• The intrinsic (mitochondrial) pathway of apoptosis depends on mitochondria and can be triggered by factors such as DNA damage, low oxygen, and low nutrients.
• Caspases 8, 9, and 10 are initiator procaspases, while caspases 3, 6, and 7 are executioner procaspases.