evaleiyuhang / parkinson

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Open evaleiyuhang opened 8 months ago

evaleiyuhang commented 8 months ago

Item 1 of 40 Foreign外来 antigen recognition at the cell surface by cytotoxic细胞毒性 T-lymphocytes stimulates a response that results in rapid cell death. Which of the following act as effectors of this response? 0 A. Matrix基质 metalloproteinases 0 B. Acid hydrolases水解酶 0 C. Caspases O D. Phospholipase A2 O E. Protein kinase A ? 0 C. Caspases (78%) The two primary modes of cell death are necrosis (which is induced by injury) and apoptosis (which is initiated by the host organism in response to cell damage, age-related atrophy, or specific stages of embryogenesis). Apoptosis is helpful in the elimination of cells that are no longer necessary and in the maintenance of a constant number of cells in rapidly growing tissues. Tumor cells, for example, die by apoptosis. The death of Band T lymphocytes and virally-infected cells also occurs through apoptosis. The remains of cells that die by this method are phagocytized by macrophages. The process of apoptosis involves the following steps:

  1. Initiation: Apoptosis is triggered by different stimuli and can occur through either the intrinsic, mitochondriamediated pathway or the extrinsic, receptor-initiated pathway. Cells damaged by ultraviolet light, heat, hypoxia, toxins, or radiation display intrinsic apoptotic signals (eg, phosphatidylserine or thrombospondin) on their plasma membranes. Extrinsic apoptosis, in contrast, is induced by the tumor necrosis factor (TNF) when bound to tumor necrosis factor receptor 1 (TNFR1) or the Fas ligand when bound to cell surface receptor Fas.
  2. Control: Intrinsic apoptosis is mediated by a group of bcl-2 proteins. Some of the components of this system are pro-apoptotic (eg, Bak, Bax, and Bim proteins), while others are anti-apoptotic (eg, Bcl-x and Bcl-2 proteins). Apoptotic signals tip the balance between these two forces, resulting in changes of the inner mitochondrial membrane. These changes are responsible for the formation of the mitochondrial permeability transition (MPT) and the release of cytochrome c and other pro-apoptotic proteins into the cytoplasm, which then activate caspases. In extrinsic apoptosis, the binding of the death ligand and the death receptor allows for pro-caspase molecules to be brought into close proximity.
  3. Destruction: Both the intrinsic and extrinsic pathways converge at this step, resulting in caspase activation. Caspases are proteolytic enzymes that destroy cell components. They contain cysteine and are able to cleave aspartic acid residues (cysteine-aspartic-acid-proteases). The eleven caspases that have been identified are classified as either initiator or effector caspases. Initiator caspases activate the effector caspases, which then cleave the cellular proteins. (Choice A) Metalloproteinases are zinc-containing enzymes that degrade the components of the extracellular matrix (eg, collagen, laminin, fibronectin). Metalloproteinases are essential for proper tissue remodeling during wound healing. (Choice B) Acid hydrolases do not participate in apoptosis. (Choice D) Phospholipase A2 does not participate in apoptosis. (Choice E) Protein kinase A is a component of the cAMP-associated signaling system. The binding of a ligand to a G-protein-l inked receptor resu lts in adenylyl cyclase activation and the release of cAMP. Elevated levels of cAMP activate protein kinase A. Educational Objective: Apoptosis can occur through either the intrinsic (mitochondria-mediated) pathway or the extrinsic (receptorinitiated) pathway. Both pathways converge in the activation of caspases. Caspases are proteolytic enzymes that cleave cellular proteins.