Cell death signaling MCQs With Answer

Cell death signaling MCQs With Answer

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Cell death signaling MCQs With Answer

Introduction: This question set is designed for M.Pharm students studying Advanced Pharmaceutical Biotechnology to deepen their understanding of regulated cell death mechanisms. The 20 multiple-choice questions focus on molecular pathways and regulatory checkpoints of apoptosis, necroptosis, pyroptosis and autophagy-related death, highlighting key proteins such as caspases, Bcl-2 family members, IAPs, RIP kinases, inflammasomes and gasdermins. Clinical and experimental implications — including small-molecule modulators, biochemical assays and therapeutic targets — are integrated to bridge basic signaling knowledge with translational pharmacology. Use these MCQs to assess comprehension and prepare for higher-level discussion and exam questions.

Q1. In the intrinsic (mitochondrial) apoptosis pathway, which event directly leads to apoptosome assembly?

  • Release of Smac/DIABLO into the cytosol
  • Translocation of Bax/Bak to the nucleus
  • Release of cytochrome c from mitochondria into the cytosol
  • Closure of the mitochondrial permeability transition pore (mPTP)

Correct Answer: Release of cytochrome c from mitochondria into the cytosol

Q2. Which Bcl-2 family proteins are primarily responsible for inducing mitochondrial outer membrane permeabilization (MOMP)?

  • Anti‑apoptotic proteins such as Bcl-2 and Bcl-xL
  • BH3-only sensitizers like Bad only
  • Multidomain pro-apoptotic effectors Bax and Bak
  • Inhibitor of apoptosis proteins (IAPs) such as XIAP

Correct Answer: Multidomain pro-apoptotic effectors Bax and Bak

Q3. Activation of which caspase is the key initiator in the extrinsic death receptor pathway leading to apoptotic execution?

  • Caspase-3
  • Caspase-8
  • Caspase-9
  • Caspase-1

Correct Answer: Caspase-8

Q4. Which molecular event explains how caspase-8 controls the choice between apoptosis and necroptosis?

  • Caspase-8 phosphorylates MLKL to activate necroptosis
  • Caspase-8 ubiquitinates RIPK1 to prevent signaling
  • Caspase-8 cleaves and inactivates RIPK1 and RIPK3
  • Caspase-8 directly activates gasdermin D

Correct Answer: Caspase-8 cleaves and inactivates RIPK1 and RIPK3

Q5. Which protein is the executioner that forms plasma membrane pores during pyroptosis following canonical inflammasome activation?

  • MLKL
  • AIF (Apoptosis-inducing factor)
  • Gasdermin D (GSDMD)
  • Cytochrome c

Correct Answer: Gasdermin D (GSDMD)

Q6. Which inflammasome sensor is most commonly associated with sensing diverse stress signals and activating caspase-1 in many inflammatory contexts?

  • RIPK3
  • NLRP3
  • Fas (CD95)
  • Atg5

Correct Answer: NLRP3

Q7. SMAC/DIABLO promotes apoptosis primarily by which mechanism?

  • Direct activation of Bax and Bak oligomerization
  • Neutralizing inhibitor of apoptosis proteins (IAPs) to permit caspase activation
  • Blocking cytochrome c release from mitochondria
  • Inhibiting caspase-8 activation at the DISC

Correct Answer: Neutralizing inhibitor of apoptosis proteins (IAPs) to permit caspase activation

Q8. Which assay combination best distinguishes early apoptosis from late apoptosis/necrosis in cultured cells?

  • TUNEL assay alone
  • Annexin V positive / Propidium iodide negative vs Annexin V positive / Propidium iodide positive
  • Measuring ATP levels only
  • Western blot for LC3-II only

Correct Answer: Annexin V positive / Propidium iodide negative vs Annexin V positive / Propidium iodide positive

Q9. Which small molecule is a selective inhibitor of RIPK1 kinase activity used to block necroptosis in experimental systems?

  • zVAD-fmk
  • Necrostatin-1
  • MCC950
  • Venetoclax

Correct Answer: Necrostatin-1

Q10. Which transcriptional target of p53 directly promotes mitochondrial apoptosis by antagonizing anti-apoptotic Bcl-2 proteins?

  • Mdm2
  • PUMA (p53 upregulated modulator of apoptosis)
  • FLIP
  • XIAP

Correct Answer: PUMA (p53 upregulated modulator of apoptosis)

Q11. Caspase-3 cleaves Poly (ADP-ribose) polymerase (PARP) during apoptosis. What is the functional consequence of PARP cleavage?

  • Enhanced DNA repair and cell survival
  • Loss of PARP enzymatic activity contributing to DNA fragmentation and energy preservation
  • Activation of necroptotic signaling via RIPK3
  • Direct inhibition of apoptosome formation

Correct Answer: Loss of PARP enzymatic activity contributing to DNA fragmentation and energy preservation

Q12. Which statement best describes the role of cFLIP within death receptor signaling?

  • cFLIP is a mitochondrial pore-forming protein causing cytochrome c release
  • cFLIP mimics caspase-8 structure and inhibits its activation at the DISC
  • cFLIP ubiquitinates TNF receptor to enhance signaling
  • cFLIP phosphorylates RIPK1 to induce necroptosis

Correct Answer: cFLIP mimics caspase-8 structure and inhibits its activation at the DISC

Q13. Which of the following best distinguishes regulated necrosis (necroptosis) from accidental necrosis?

  • Necroptosis requires mitochondrial cytochrome c release.
  • Necroptosis is an ATP-independent passive process.
  • Necroptosis is a programmed process mediated by defined signaling molecules such as RIPK1, RIPK3 and MLKL.
  • Necroptosis is inhibited by activation of gasdermin D.

Correct Answer: Necroptosis is a programmed process mediated by defined signaling molecules such as RIPK1, RIPK3 and MLKL.

Q14. Which molecular event is essential for MLKL to execute plasma membrane disruption during necroptosis?

  • Ubiquitination of MLKL by cIAPs
  • Phosphorylation of MLKL by RIPK3 leading to MLKL oligomerization and membrane translocation
  • Cleavage of MLKL by caspase-3
  • Binding of MLKL to mitochondrial cardiolipin

Correct Answer: Phosphorylation of MLKL by RIPK3 leading to MLKL oligomerization and membrane translocation

Q15. In the context of endoplasmic reticulum (ER) stress, which UPR branch primarily mediates CHOP induction and pro-apoptotic signaling?

  • IRE1α → XBP1s splicing only
  • PERK → eIF2α phosphorylation leading to ATF4 and CHOP induction
  • ATG7-dependent autophagy activation
  • ATF6 cleavage leading exclusively to autophagy

Correct Answer: PERK → eIF2α phosphorylation leading to ATF4 and CHOP induction

Q16. Which therapeutic agent is a BH3-mimetic used clinically to antagonize Bcl-2 and induce apoptosis in certain hematological malignancies?

  • MCC950
  • Venetoclax
  • Necrostatin-1
  • zVAD-fmk

Correct Answer: Venetoclax

Q17. Which caspase is primarily involved in canonical inflammatory cytokine maturation (IL-1β and IL-18) downstream of inflammasome activation?

  • Caspase-3
  • Caspase-8
  • Caspase-1
  • Caspase-9

Correct Answer: Caspase-1

Q18. Which experimental readout specifically measures mitochondrial outer membrane permeabilization (MOMP) rather than downstream caspase activation?

  • Cleavage of PARP detected by Western blot
  • Release of cytochrome c from mitochondria to cytosol detected by subcellular fractionation
  • Annexin V staining only
  • Measurement of caspase-3 activity with fluorogenic substrate

Correct Answer: Release of cytochrome c from mitochondria to cytosol detected by subcellular fractionation

Q19. Which post-translational modification of RIPK1 is critical for suppressing its pro-death signaling in the TNF receptor complex I?

  • Phosphorylation by caspase-8
  • K63-linked ubiquitination by cIAPs
  • Sumoylation by SUMO1 exclusively
  • Acetylation at the BH3 domain

Correct Answer: K63-linked ubiquitination by cIAPs

Q20. Which mechanism explains how SMAC mimetics can sensitize cancer cells to TNFα-induced cell death?

  • SMAC mimetics increase Bcl-2 expression to promote apoptosis
  • SMAC mimetics stabilize XIAP to block caspases
  • SMAC mimetics promote degradation of cIAPs, altering TNF signaling to favor cell death
  • SMAC mimetics directly inhibit MLKL phosphorylation

Correct Answer: SMAC mimetics promote degradation of cIAPs, altering TNF signaling to favor cell death

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