Caspases

Definition

Caspases are a family of cysteine proteases that play essential roles in programmed cell death (apoptosis) and inflammation. They are synthesized as inactive precursors and are activated in response to various cellular signals, leading to the cleavage of specific substrates that ultimately result in cellular breakdown and inflammation regulation.

5 Must Know Facts For Your Next Test

1. Caspases are categorized into two main groups: initiator caspases (like caspase-8 and caspase-9) that start the apoptotic process, and executioner caspases (like caspase-3 and caspase-7) that carry out the death program by degrading cellular components.
2. They can be activated through intrinsic pathways (mitochondrial stress) or extrinsic pathways (death receptor signaling), highlighting their role in responding to various cellular stressors.
3. Caspases not only mediate apoptosis but also have functions in inflammation, where they can cleave pro-inflammatory cytokines, thus amplifying the immune response.
4. Dysregulation of caspase activity is linked to several diseases, including cancer, neurodegenerative disorders, and autoimmune diseases, making them a target for therapeutic interventions.
5. Calcium ions can influence caspase activation, as fluctuations in intracellular calcium levels are known to affect the signaling pathways that lead to apoptosis.

Review Questions

• How do caspases function as both initiators and executioners in the process of apoptosis?
  • Caspases function in two main roles within apoptosis: initiators and executioners. Initiator caspases, such as caspase-8 and caspase-9, respond to specific signals that trigger the apoptotic cascade. Once activated, they cleave and activate executioner caspases like caspase-3 and caspase-7. These executioner caspases then carry out the death program by degrading crucial cellular proteins, ultimately leading to cell dismantling.
• Discuss the relationship between intracellular calcium dynamics and the activation of caspases during apoptosis.
  • Intracellular calcium levels play a significant role in the activation of caspases during apoptosis. An increase in intracellular calcium can trigger various signaling pathways that lead to the activation of initiator caspases. This elevated calcium can also affect mitochondrial function, which releases cytochrome c that further activates downstream executioner caspases. Thus, calcium dynamics directly influence how cells respond to stress signals by promoting apoptosis through the activation of caspases.
• Evaluate how the dysregulation of caspase activity can contribute to disease states, particularly in cancer and neurodegenerative disorders.
  • The dysregulation of caspase activity can significantly contribute to various disease states such as cancer and neurodegenerative disorders. In cancer, the inhibition of apoptotic pathways often occurs, allowing abnormal cells to survive longer than they should due to reduced caspase activity. Conversely, excessive activation of caspases can lead to neurodegeneration, where unintended cell death results in loss of neuronal function. Understanding these dysregulated processes provides insight into potential therapeutic approaches targeting caspases for treatment strategies across different diseases.

Related terms

Apoptosis: A regulated process of programmed cell death that eliminates damaged or unwanted cells without causing inflammation.

Inflammation: The body's response to injury or infection, which can involve the activation of immune cells and the release of signaling molecules.

Procaspases: Inactive precursors of caspases that undergo proteolytic cleavage to become active caspases in response to pro-apoptotic signals.