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Apoptosis (presentation)
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Apoptosis (presentation)


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  • Before we go on, let look at the way cell dies There are different ways a cell die Necrosis (in Greek Νεκρός = Dead ) is the name given to accidental death of cells and living tissue .
  • Transcript

    • 1. By: Thinh Le
    • 2. Introduction
      • The word apoptosis was introduced by Kerr, Wyllie and Currie to describe a form of cell death distinct from necrosis.
      • Apo = [ Greek ] : from, separation from; Ptosis= [ Greek ] : dropping, a falling down
    • 3. Apoptosis vs Necrosis Apoptosis • Chromatin condensation • Cell Shrinkage • Preservation of Organelles and cell membranes • Rapid engulfment by neighboring cells preventing inflammation Necrosis • Nuclear swelling • Cell Swelling • Disruption of Organelles • Rupture of cell and release of cellular contents • Inflammatory response 1972 Kerr Wyllie Currie
    • 4. Evolution of the Origin of Programmed Cell Death (PCD)
      • Mitochondria retain their collection of molecule that can trigger cell suicide after the enter the stabilize in the eukaryotic cell.
      • This process has evolved to occur only when programmed.
    • 5. Purpose of Apoptosis
      • It’s essential for the proper development and to maintain homeostasis for the organism.
    • 6. Inititation
      • DNA damage within the cell.
      • Cancerous cells
      • Cells of the immune system after they have fulfilled their function
      • Ionizing Radiation
      • Stress and infection such as virus
      Types of Induction: Cell surface death receptor mediated pathway (extrinsic) Mitochondrial-initiated pathway (intrinsic)
    • 7.  
    • 8. Caspases
      • Family of Proteins- main executors of the apoptotic process.
      • They belong to a group of enzymes known as cysteine proteases.
        • Zymogens- inactive forms
      • Caspase 8 and 10- initiator (extrinsic)
      • Caspase 9- initiator (intrinsic)
        • Lead to effector caspase 3 and 6
          • Cleave key cellular proteins
    • 9. Other Important Proteins
      • Blc-2 family helps regulate the activation of procaspases.
        • Inhibitors - Bcl-2, Bcl-X L
        • Promoters – Bad, Bax, Bak
    • 10. Mechanism (Extrinsic)
      • Death Receptors- cell surface receptor that transmit apoptotic signals, initiated by ligands.
        • Ligands: Fas ligand, Tumor Necrosis Factor (TNF) alpha, and Tumor necrosis (TNF)-related apoptosis-inducing ligand TRAIL.
      • Lead to generation of ceramide
        • Result in large number of clustering of death receptors.
          • This helps strengthen the apoptotic signaling.
      • Death domain
        • Conformation change in the intracellular domain of the receptor.
        • Allows recruitment of various apoptotic proteins to the receptor.
    • 11. Death Inducing Signaling Complex
    • 12. Mechanism (Extrinsic) cont.
      • Final step- recruitment of caspase 8
        • Resulting the activation of caspase 8 and the initiation of apoptosis.
    • 13. Mechanism (Extrinsic) cont.
    • 14. Mechanism (Intrinsic)
      • Mitochondria contains proteins like Apoptosis Inducing Factor (AIF), Smac/ DIABLO and Cytochrome C that regulate cell death.
      • These proteins are release through the a pore called Permeability Transition (PT) pore
        • Form by pro-apoptotic members of Bcl-2 family (activated by apoptotic signals)
      • The release of Cytochrome leads to recruitment of pro-caspase 9 and Apoptotic protease activating factor 1 ( Apaf-1).
        • This forms the apoptosome
    • 15.  
    • 16. Mechanism (Intrinsic) cont.
      • This is follow by the activation of caspase 9 which in turn result with the induction of apoptosis.
    • 17. Mechanism (Intrinsic) cont.
    • 18. Review
    • 19. Conclusion
    • 20. References
      • Albanese, Joseph, Nicholas D. Ionizing Radiation Alters Fas Antigen Ligand at the Cell Surface and on Exfoliated Plasma Membrane-Derived Vesicle: Implications for Apoptosis and Intercellular Signaling . Yale University School of Medicine. Radiation Research pg. 49-61 (2000)
      • Alberts, Bruce, Alexander J., Julian L., Martin R., Keith R., Peter W. Molecular Biology of The Cell 4 th Edition. Garland Science. pg. 1010-1014. Chiarugi and Moskowitz. PARP-1--a perpetrator of apoptotic cell death? Science 297, p. 2008
      • Almasan, Alex. Cellular Commitment to Radiation-Induction Apoptosis . Department of Cancer Biology. pg. 347-350 Vol. 153 Issue 3 (March 2000)
      • Bruchhaus, Iris. Protozoan parasites: Programmed Cell Death as a Mechanism of parasitism . Bernhard Nocht Inst. Trop. Medicine. Trends in Parasitology 23, no. 8 (August 2007):376-383
      • Ejima, Kuniaki. Inductionn of Apoptosis in Placentas of Pregnant Mice Exposed to Lipopolysaccharides: Possible Involvement of Fas/Fas Ligand System. University of Occupational and Environmental Health. Biology of Reproduction 62, 178-185 . 17 May 1999.
      • Park, HeonJoo. Apoptosis and Cell Cycle Progression in an Acidic Environment After Irradiation . University of Minnesota Medical School. Radiation Research pg. 295-304 vol. 153:3 (March 2000)