Cell Signalling Part 1 Test

1. Which molecule acts as a molecular switch by cycling between active and inactive forms in signalling?

2. Loss of function mutation in Axin will lead to:

3. Which evidence supports that MAPK signalling requires sequential phosphorylation cascade?

4. A JAK mutant cannot phosphorylate STAT but can still autophosphorylate. Which outcome will occur?

5. If β-arrestin is absent in GPCR signalling, what will happen?

6. Which experimental approach proves that cAMP is a second messenger?

7. What is the immediate effect of insulin binding to its receptor?

8. A cancer cell line shows a mutation in PI3K that makes it constitutively active. Which drug will block tumour survival most directly?

9. Which event is essential for STAT nuclear translocation?

10. Cells treated with phosphodiesterase inhibitor show prolonged cAMP signals. Which interpretation is correct?

11. Which of the following is a common property of both GPCR and RTK signalling?

12. An RTK inhibitor prevents autophosphorylation but receptor dimerization is unaffected. Which downstream event will be blocked?

13. Which signalling pathway involves SMAD proteins?

14. A Hedgehog pathway mutant has Smoothened locked in an inactive state. What will be the outcome?

15. Which experiment best demonstrates cross-talk between PI3K-Akt and MAPK pathways?

16. Treatment of cells with a proteasome inhibitor will affect which signalling pathway most directly?

17. In a mutant lacking functional IP3 receptor, stimulation of PLC pathway results in:

18. Ras has a mutation preventing GTP hydrolysis. What is the cellular consequence?

19. A small molecule inhibitor blocks calmodulin function. Which signalling outcome is directly affected?

20. A GPCR mutant cannot hydrolyze GTP bound to Gα subunit. What is the most likely outcome?

21.

A researcher investigates MAPK signalling:

• EGF activates ERK phosphorylation.

• Ras inhibitor abolishes ERK activation.

• Raf inhibitor abolishes ERK activation.

• PI3K inhibitor has no effect on ERK activation.

Which pathway is confirmed?

22.

An experiment tracks nuclear translocation of β-catenin in cells treated with different inhibitors:

• GSK-3β inhibitor → β-catenin nuclear localization ↑

• Proteasome inhibitor → β-catenin accumulates but no nuclear entry

• Axin overexpression → β-catenin levels ↓

Which is the correct interpretation?

23. A cancer cell line shows constitutive activation of Akt. Which intervention would MOST directly block this effect?

24. In Hedgehog signalling, a mutation leads to constant activation of Gli transcription factor even in the absence of ligand. Which mutation is most likely responsible?

25.

An experiment involves mutating the SH2 domain of STAT proteins. Results show:

• STATs are still phosphorylated by JAKs.

• STATs fail to dimerize.

• No nuclear translocation observed.

Which conclusion is correct?

26.

A researcher studies Ca²⁺ signalling in neurons. The following data are observed:

1. Blocking extracellular Ca²⁺ entry has little effect.

2. Blocking SERCA pump abolishes Ca²⁺ transients.

3. Addition of IP3 mimics neurotransmitter action.

Which interpretation is most accurate?

27.

During NF-κB activation:

• In resting cells, NF-κB is bound to IκB in cytoplasm.

• Upon TNF-α stimulation, IKK complex phosphorylates IκB.

• A proteasome inhibitor is added experimentally.

Predict the outcome:

28.

In Wnt signalling, β-catenin stability is crucial. A researcher performs knockouts:

• KO of Dishevelled (Dvl) → β-catenin degraded.

• KO of GSK-3β → β-catenin stabilized even without Wnt.

• KO of APC → constitutive β-catenin stabilization.

• KO of Frizzled receptor → β-catenin degraded.

Which combination of results best demonstrates that the destruction complex negatively regulates β-catenin?

29.

An experiment tests the effect of mutating tyrosine residues on the cytoplasmic tail of an RTK. Cells expressing mutant receptors show:

• Receptor dimerization and autophosphorylation occurs normally.

• Grb2 binding is abolished.

• Ras activation is lost.

• PI3K can still bind to receptor.

Which statement explains the observations best?

30.

A novel peptide hormone "X" is discovered. When it binds to its receptor on the plasma membrane, the following experimental results are observed:

1. Increase in intracellular cAMP levels.

2. No increase in IP3 or DAG.

3. Pretreatment with cholera toxin (CT) exaggerates the effect of hormone X.

4. Pretreatment with pertussis toxin (PTX) does not affect the response.

Based on these results, which conclusion is most accurate?

31. Which experimental approach would best establish that JAK is essential for STAT activation?

32. A small molecule drug inhibits PI3K activity. Which downstream event is most likely blocked?

33. In NF-κB signalling, which event occurs immediately after receptor stimulation?

34. A researcher mutates the SH2 domain of Grb2 adaptor protein. Which pathway will be directly affected?

35. Which of the following experimental observations supports the role of calmodulin in Ca²⁺ signalling?

36. During Wnt signalling, β-catenin is stabilized. Which of the following proteins is directly involved in preventing β-catenin degradation?

37. A growth factor activates RTK (Receptor Tyrosine Kinase). Which of the following experimental results would best demonstrate that the downstream signalling involves the Ras-MAPK cascade?

38. A mutant cell line has a defective phospholipase C (PLC). Which signalling pathway will be directly affected?

39. Which one of the following is NOT a second messenger in cell signalling?

40. A G-protein coupled receptor (GPCR) is activated by binding of a hormone. Which of the following sequence correctly represents the events leading to cellular response?