Hormone Biochemistry and Signal Transduction MCQs

Biochemistry · 43 free questions with answers & explanations.

1. A Gs-coupled receptor on a hepatocyte is activated. The effector pathway that is directly activated by GTP-bound Gsα is:
2. Insulin receptor signalling activates PI3K/Akt pathway. Which immediate downstream substrate of Akt is phosphorylated to allow GLUT4 vesicle fusion with the plasma membrane in adipocytes?
3. A patient is found to have pseudohypoparathyroidism type 1a (Albright's hereditary osteodystrophy). The molecular defect is a loss-of-function mutation in:
4. Steroid hormones exert their genomic effects via nuclear receptors. Which domain of a nuclear receptor directly contacts the specific DNA sequence (hormone response element)?
5. Cholera toxin causes persistent diarrhoea by ADP-ribosylating which protein, and what is the functional consequence?
6. A patient with McCune-Albright syndrome has autonomous hormone hypersecretion in multiple endocrine glands without ligand stimulation. The molecular defect is a gain-of-function mutation in which protein?
7. Insulin receptor signaling activates IRS-1 → PI3K → PIP3 → PDK1 → Akt pathway. Which downstream effect of Akt is responsible for acute GLUT4 translocation to the plasma membrane in muscle?
8. A drug that acts as a PPAR-gamma (peroxisome proliferator-activated receptor gamma) agonist would mimic which class of antidiabetic agents, and through which mechanism?
9. Pertussis toxin catalyzes ADP-ribosylation of Gi-alpha, rendering it permanently inactive. What would be the expected effect on cAMP levels in cells where Gi-coupled receptors are normally inhibitory?
10. Steroid hormone receptors, when unliganded, are retained in the cytoplasm by heat shock proteins. Upon ligand binding, the receptor undergoes which sequence of events to regulate gene transcription?
11. A patient with McCune-Albright syndrome has constitutively active Gs-alpha protein in multiple tissues. Which of the following signal transduction components is DIRECTLY activated by this mutant Gs-alpha?
12. Insulin binds to its receptor and activates downstream glucose uptake. The IMMEDIATE biochemical consequence of insulin binding to its receptor tyrosine kinase is:
13. A researcher finds that a novel drug blocks the action of phosphodiesterase-5 (PDE5) in vascular smooth muscle. The resulting clinical effect is vasodilation. The biochemical mechanism is:
14. Which hormone uses an intracellular receptor that, after ligand binding, acts as a transcription factor by binding to hormone response elements (HREs) in target gene promoters?
15. A patient with Pseudohypoparathyroidism type 1a (PHP-1a) has elevated PTH but hypocalcaemia. The primary biochemical defect is:
16. Insulin receptor tyrosine kinase autophosphorylates upon insulin binding. The primary immediate downstream substrate of activated insulin receptor kinase that initiates the PI3K-Akt pathway is:
17. A research study demonstrates that a Gs protein-coupled receptor agonist increases cAMP. The elevated cAMP activates PKA, which phosphorylates CREB. What is the direct molecular consequence of CREB phosphorylation at Ser133?
18. A 28-year-old woman is diagnosed with pseudohypoparathyroidism type Ia (Albright hereditary osteodystrophy). Labs show hypocalcemia, hyperphosphatemia, and elevated PTH. The underlying molecular defect is:
19. Glucagon activates glycogen phosphorylase in hepatocytes through a second messenger cascade. The rate-limiting amplification step in this cascade, making even nanomolar glucagon concentrations effective, is:
20. Thyroid hormones (T3) exert their genomic effects by binding to thyroid hormone receptor (TR). Before T3 binding, TR bound to thyroid response elements (TRE) on DNA is associated with co-repressors. This pre-ligand complex actively represses transcription by:
21. Insulin signalling activates PI3K, which phosphorylates PIP2 to PIP3. PIP3 recruits PDK1, which activates Akt (PKB). The PRINCIPAL metabolic consequence of this Akt activation in adipose tissue is:
22. Thyroid hormone (T3) enters the nucleus and binds thyroid hormone receptor (TR), which is constitutively bound to DNA as a heterodimer with RXR. In the ABSENCE of T3, this complex:
23. A patient with McCune-Albright syndrome has constitutively active Gs-alpha protein due to a somatic mutation at Arg201. The DIRECT biochemical consequence in the affected cells is:
24. Glucagon binds its GPCR on hepatocytes. The subsequent activation of PKA phosphorylates phosphofructokinase-2 (PFK-2/FBPase-2 bifunctional enzyme). The NET metabolic effect of this phosphorylation is:
25. A pharmaceutical company develops an antagonist that blocks the beta-arrestin recruitment to beta2-adrenergic receptors while leaving G-protein coupling intact. The clinical consequence would be:
26. Glucagon binds its GPCR on hepatocytes. The immediate downstream consequence that activates protein kinase A (PKA) is production of which second messenger?
27. A child with features of Albright hereditary osteodystrophy (short stature, short 4th metacarpal, subcutaneous ossifications) has elevated PTH with hypocalcaemia but a normal PTH receptor gene. The molecular defect most likely involves:
28. Insulin receptor tyrosine kinase autophosphorylation triggers a signalling cascade culminating in translocation of which glucose transporter to the plasma membrane of adipocytes and skeletal muscle?
29. Steroid hormones exert their principal genomic effects by binding to nuclear receptors that act as ligand-activated transcription factors. Which structural domain of the nuclear receptor directly contacts the hormone response element (HRE) on DNA?
30. A 28-year-old woman with features of hyperthyroidism is found to have TSH receptor-stimulating antibodies (TRAb). These antibodies mimic TSH by acting on a receptor coupled to which intracellular signalling mechanism?
31. Insulin stimulates glucose uptake in adipocytes primarily by:
32. A patient with pseudohypoparathyroidism type 1a has hypocalcaemia and elevated PTH but shows no response to exogenous PTH. The molecular defect is in:
33. Which second messenger is generated by phospholipase C acting on PIP2, and directly causes calcium release from the endoplasmic reticulum?
34. Glucagon's ability to stimulate hepatic glycogenolysis is mediated by the sequence:
35. Nitric oxide (NO) synthesized by endothelial NOS causes vascular smooth muscle relaxation by activating:
36. A constitutively active RAS mutation found in 30% of human cancers leads to uncontrolled cell proliferation because:
37. Steroid hormones differ from peptide hormones in their mechanism of action because steroids:
38. Insulin signalling activates PI3K → PIP3 → PDK1 → Akt (PKB) pathway. Akt phosphorylates and inactivates glycogen synthase kinase-3 (GSK-3), thereby activating glycogen synthase. The additional mechanism by which insulin simultaneously promotes glycogen synthesis via protein phosphatase-1 (PP1) activation is:
39. A patient with McCune-Albright syndrome has constitutively active Gs-alpha protein in multiple tissues due to a somatic activating mutation. The biochemical consequence of a constitutively active Gs-alpha is:
40. Thyroid hormone T3 (triiodothyronine) exerts its genomic effects by acting as a ligand for nuclear thyroid hormone receptors (TR). Before ligand binding, the unliganded TR/RXR heterodimer on thyroid hormone response elements (TREs) typically:
41. Glucocorticoids exert anti-inflammatory effects partly through non-genomic mechanisms (protein-protein interactions), particularly by inhibiting transcription factors. The key transcription factor that glucocorticoid receptor (GR) directly inhibits through protein-protein interaction (transrepression) in inflammation is:
42. Parathyroid hormone (PTH) binds the PTH1 receptor (PTH1R), a Gs- and Gq-coupled GPCR. In chronic kidney disease (CKD), secondary hyperparathyroidism develops. The initial biochemical trigger in CKD that drives increased PTH secretion is:
43. Diabetes insipidus (DI) is characterised by the inability to concentrate urine. Central DI results from ADH (vasopressin) deficiency; nephrogenic DI results from resistance to ADH. ADH acts on principal cells of the collecting duct via V2 receptor coupled to Gs. The intracellular signalling pathway that leads to insertion of aquaporin-2 (AQP2) into the apical membrane is: