Enzyme-Linked Receptors — MCQs

10 questions

Match the following drugs with the targets of their actions: Drugs: A. Trastuzumab B. Infliximab C. Sirolimus D. Imatinib Targets: 1. BCR-ABL tyrosine kinase 2. mTOR 3. TNF alpha 4. HER2/neu

Which hormone acts on JAK-STAT kinase receptor?

Which of the following is true? 1. BRCA1 is an oncogene 2. HER2neu is amplified only in a fraction of breast cancer 3. EGFR (+) is seen in non-small cell lung cancer 4. N-MYC is a tumor suppressor gene

What type of receptor is the insulin receptor?

Which of the following statements best describes the mechanism of action of insulin on target cells?

Agent that acts through tyrosine kinase receptor is

In response to changes in Ca2+ concentration, which of the following Ca2+ binding proteins can modify the activity of many enzymes & proteins?

Which enzyme is responsible for the activation of Interleukin-1 (IL-1)?

Which amino acid can be utilized in both gluconeogenesis and ketogenesis?

Q10

Which of the following binds to Tyrosine Kinase receptor?

Enzyme-Linked Receptors Indian Medical PG Practice Questions and MCQs

Question 1: Match the following drugs with the targets of their actions: Drugs: A. Trastuzumab B. Infliximab C. Sirolimus D. Imatinib Targets: 1. BCR-ABL tyrosine kinase 2. mTOR 3. TNF alpha 4. HER2/neu

A. A-2, B-3, C-1, D-4
B. A-3, B-4, C-2, D-1
C. A-4, B-3, C-1, D-2
D. A-4, B-3, C-2, D-1 (Correct Answer)

Explanation: ***Correct Answer: A-4, B-3, C-2, D-1*** - **Trastuzumab** (Herceptin) is a **monoclonal antibody** that targets the **HER2/neu receptor (4)** [1], [2], commonly overexpressed in certain breast cancers and gastric cancers. - **Infliximab** is another **monoclonal antibody** that specifically targets and neutralizes **TNF-alpha (3)**, an inflammatory cytokine, making it useful in treating autoimmune diseases like rheumatoid arthritis and Crohn's disease. - **Sirolimus** is an **immunosuppressant** drug that inhibits the mammalian target of rapamycin (**mTOR (2)**), a protein kinase involved in cell growth and proliferation, used in transplant medicine and as an anticancer agent. - **Imatinib** is a **tyrosine kinase inhibitor** that primarily targets the **BCR-ABL fusion protein (1)** [1], [2], which is characteristic of chronic myeloid leukemia. *Incorrect: A-2, B-3, C-1, D-4* - This option incorrectly matches Trastuzumab with mTOR and Sirolimus with BCR-ABL, which are not their primary targets. - Trastuzumab targets HER2/neu [1], [2], and Sirolimus targets mTOR. *Incorrect: A-3, B-4, C-2, D-1* - This option incorrectly matches Trastuzumab with TNF-alpha and Infliximab with HER2/neu. - Infliximab targets TNF-alpha, and Trastuzumab targets HER2/neu [1], [2]. *Incorrect: A-4, B-3, C-1, D-2* - This option incorrectly matches Sirolimus with BCR-ABL and Imatinib with mTOR. - Sirolimus inhibits mTOR, and Imatinib inhibits BCR-ABL [1], [2].

Question 2: Which hormone acts on JAK-STAT kinase receptor?

A. TSH
B. Thyroxine
C. GH (Correct Answer)
D. FSH

Explanation: ***GH*** - **Growth Hormone (GH)** binds to a **cytokine receptor** that lacks intrinsic tyrosine kinase activity and instead signals through associated **JAK-STAT kinases**. - This binding leads to **JAK phosphorylation**, which then phosphorylates and activates **STAT proteins**, regulating gene expression. *TSH* - **Thyroid-stimulating hormone (TSH)** acts on a **G protein-coupled receptor** to stimulate thyroid hormone production and release. - Its signaling pathway primarily involves the activation of **adenylyl cyclase** and increases in **cAMP**, not the JAK-STAT pathway. *Thyroxine* - **Thyroxine (T4)** is a **thyroid hormone** that primarily acts by binding to **intracellular nuclear receptors**, which then regulate gene transcription. - It directly influences gene expression, rather than signaling through cell surface receptors and kinase pathways like JAK-STAT. *FSH* - **Follicle-stimulating hormone (FSH)**, like TSH, signals through a **G protein-coupled receptor** on target cells in the gonads. - This activation primarily leads to an increase in **intracellular cAMP levels** to mediate its effects on gamete production and hormone synthesis.

Question 3: Which of the following is true? 1. BRCA1 is an oncogene 2. HER2neu is amplified only in a fraction of breast cancer 3. EGFR (+) is seen in non-small cell lung cancer 4. N-MYC is a tumor suppressor gene

A. 1,3
B. 1,2
C. 2,3 (Correct Answer)
D. All of the options

Explanation: ***Correct Option: 2,3*** - **Statement 2 is TRUE**: HER2neu amplification occurs in only a fraction (~15-20%) of breast cancers, making it a specific subset requiring targeted therapy with trastuzumab (Herceptin) [1]. - **Statement 3 is TRUE**: EGFR (epidermal growth factor receptor) mutations or overexpression are commonly seen in non-small cell lung cancer (NSCLC) and serve as important therapeutic targets for tyrosine kinase inhibitors. *Incorrect Option: 1,3* - Statement 1 is **FALSE**: BRCA1 is a **tumor suppressor gene**, not an oncogene. It functions in DNA double-strand break repair, and loss-of-function mutations increase the risk of breast and ovarian cancers. - Statement 3 is TRUE, but the inclusion of the false statement about BRCA1 makes this option incorrect. *Incorrect Option: 1,2* - Statement 1 is **FALSE**: BRCA1 is a **tumor suppressor gene**, not an oncogene. - Statement 2 is TRUE [1], but the false classification of BRCA1 invalidates this option. *Incorrect Option: All of the options* - Statement 1 is **FALSE**: BRCA1 is a tumor suppressor gene, not an oncogene. - Statement 4 is **FALSE**: N-MYC is an **oncogene** that is amplified in neuroblastoma and other cancers, not a tumor suppressor gene. - Since two of the four statements are incorrect, "All of the options" cannot be true. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1059-1060.

Question 4: What type of receptor is the insulin receptor?

A. Guanylyl cyclase
B. Adenylyl cyclase
C. IP3-DAG
D. Tyrosine kinase (Correct Answer)

Explanation: ***Tyrosine kinase*** - The insulin receptor is a **receptor tyrosine kinase (RTK)**, meaning it has intrinsic tyrosine kinase activity that phosphorylates specific tyrosine residues on itself and other intracellular proteins upon insulin binding. - This phosphorylation initiates a **signaling cascade** involving molecules like IRS proteins, PI3K/Akt, and MAPK pathways, leading to glucose uptake and metabolic regulation. *Guanylyl cyclase* - Guanylyl cyclase receptors, such as the **atrial natriuretic peptide receptor**, catalyze the conversion of GTP to **cGMP**, which acts as a second messenger. - This mechanism is distinct from the insulin receptor's direct protein phosphorylation. *Adenylyl cyclase* - Adenylyl cyclase is typically activated by **G-protein coupled receptors (GPCRs)**, leading to the conversion of ATP to **cAMP**, another second messenger. - The insulin receptor does not couple to G proteins or directly activate adenylyl cyclase. *IP3-DAG* - The **inositol triphosphate (IP3)** and **diacylglycerol (DAG)** pathway is primarily activated by certain **GPCRs** and involves the hydrolysis of PIP2 by phospholipase C, leading to calcium release and protein kinase C activation. - This pathway is not the primary signaling mechanism initiated by the insulin receptor.

Question 5: Which of the following statements best describes the mechanism of action of insulin on target cells?

A. Insulin binds to a receptor on the outer surface of the plasma membrane, activating adenylate cyclase through the Gs protein.
B. Insulin binds to a cytoplasmic receptor and is transferred as a hormone receptor complex to the nucleus to modulate gene expression.
C. Insulin enters the cell and causes the release of calcium ions from intracellular stores.
D. Insulin binds to a transmembrane receptor on the outer surface of the plasma membrane, activating the tyrosine kinase in the cytosolic domain of the receptor. (Correct Answer)

Explanation: ***Insulin binds to a transmembrane receptor on the outer surface of the plasma membrane, activating the tyrosine kinase in the cytosolic domain of the receptor.*** - **Insulin** is a **peptide hormone** and cannot freely pass through the lipid bilayer, thus it binds to a **transmembrane receptor** on the cell surface. - This binding leads to the activation of the receptor's intrinsic **tyrosine kinase activity** in the intracellular domain, initiating a signaling cascade. *Insulin binds to a cytoplasmic receptor and is transferred as a hormone receptor complex to the nucleus to modulate gene expression.* - This mechanism describes the action of **steroid hormones**, which are lipid-soluble and can cross the cell membrane, binding to **intracellular receptors**. - **Insulin** acts via a **cell surface receptor** and its downstream effects are mediated through signal transduction pathways, not direct nuclear translocation. *Insulin binds to a receptor on the outer surface of the plasma membrane, activating adenylate cyclase through the Gs protein.* - This mechanism is characteristic of **G-protein coupled receptors (GPCRs)**, which activate or inhibit enzymes like adenylate cyclase via G-proteins to produce second messengers like cyclic AMP. - The **insulin receptor** is a **receptor tyrosine kinase**, not a GPCR, and does not directly activate adenylate cyclase via Gs protein. *Insulin enters the cell and causes the release of calcium ions from intracellular stores.* - While some hormones and neurotransmitters can trigger the release of intracellular **calcium ions**, this is typically mediated by specific pathways (e.g., GPCRs linked to phospholipase C). - **Insulin** does not directly enter target cells to cause calcium release; its actions are primarily mediated through receptor tyrosine kinase signaling pathways.

Question 6: Agent that acts through tyrosine kinase receptor is

A. Insulin (Correct Answer)
B. MSH
C. TSH
D. TRH

Explanation: ***Insulin*** - **Insulin** binds to its receptor, which is a **tyrosine kinase receptor**, leading to autophosphorylation and the activation of intracellular signaling pathways. - This activation is crucial for glucose uptake and metabolism by various cells in the body. *MSH* - **Melanocyte-stimulating hormone (MSH)** acts primarily through **G protein-coupled receptors**, specifically melanocortin receptors. - These receptors activate adenylyl cyclase, leading to an increase in intracellular cAMP. *TSH* - **Thyroid-stimulating hormone (TSH)** also acts via a **G protein-coupled receptor** on thyroid follicular cells. - Its binding stimulates adenylyl cyclase, increasing cAMP and thus thyroid hormone synthesis and release. *TRH* - **Thyrotropin-releasing hormone (TRH)** binds to **G protein-coupled receptors** on pituitary thyrotrophs. - This interaction activates the phospholipase C pathway, leading to the release of TSH.

Question 7: In response to changes in Ca2+ concentration, which of the following Ca2+ binding proteins can modify the activity of many enzymes & proteins?

A. Collagen
B. Calmodulin (Correct Answer)
C. Kinesin
D. Elastin

Explanation: ***Calmodulin*** - **Calmodulin** is a highly conserved, 148-amino acid protein with four **calcium-binding EF-hand motifs**. - Upon binding to **calcium ions (Ca2+)**, it undergoes a conformational change that enables it to interact with and regulate the activity of a wide variety of enzymes and proteins, including **kinases, phosphatases, and ion channels**, mediating many Ca2+-dependent cellular processes. *Collagen* - **Collagen** is a major structural protein in the extracellular matrix, providing **tensile strength** to tissues. - Its primary function is structural support, rather than acting as a calcium-sensing regulatory protein for enzyme activity. *Kinesin* - **Kinesin** is a **motor protein** involved in intracellular transport, moving cargo along microtubules. - While its activity can be modulated, it is not primarily known as a calcium-binding protein that directly regulates a broad range of enzymes in response to calcium concentration changes. *Elastin* - **Elastin** is a highly elastic protein found in connective tissue, allowing tissues to **recoil after stretching**. - Like collagen, its main role is structural, contributing to the elasticity of tissues, rather than signaling or enzyme regulation via calcium binding.

Question 8: Which enzyme is responsible for the activation of Interleukin-1 (IL-1)?

A. Caspase 1 (Correct Answer)
B. Caspase 3
C. Caspase 8
D. Caspase 5

Explanation: ***Caspase 1*** - **Caspase 1**, also known as **IL-1 beta converting enzyme (ICE)**, is primarily responsible for cleaving the inactive precursor forms of **pro-IL-1β** and **pro-IL-18** into their active, mature forms. - Its activation is a crucial step in the **inflammasome pathway**, mediating the inflammatory response. *Caspase 3* - **Caspase 3** is a key executioner caspase in **apoptosis**, responsible for cleaving numerous cellular proteins, leading to cell death. - It does not directly activate IL-1; its primary role is in programmed cell death, not cytokine maturation. *Caspase 8* - **Caspase 8** is an initiator caspase involved in the **extrinsic pathway of apoptosis**, activated by death receptor signaling. - While it plays a role in some inflammatory processes, it is not directly involved in the proteolytic activation of IL-1. *Caspase 5* - **Caspase 5** is an inflammatory caspase that can be activated by the inflammasome, but its role in IL-1 processing is considered minor compared to **Caspase 1**. - Its primary function is less directly involved in the central activation of IL-1β.

Question 9: Which amino acid can be utilized in both gluconeogenesis and ketogenesis?

A. Leucine
B. Valine
C. Arginine
D. Tyrosine (Correct Answer)

Explanation: ***Tyrosine (Correct Answer)*** - Tyrosine is **both glucogenic and ketogenic**, making it the correct answer. - It is **glucogenic** because its metabolism yields **fumarate**, which can enter the TCA cycle and contribute to **gluconeogenesis**. - It is also **ketogenic** because its degradation produces **acetoacetate**, a **ketone body**. *Leucine* - Leucine is a purely **ketogenic** amino acid, meaning its catabolism only produces **acetyl-CoA** and **acetoacetate**. - It cannot be converted into glucose precursors and therefore does not contribute to gluconeogenesis. *Valine* - Valine is a purely **glucogenic** amino acid, meaning its metabolism produces **succinyl-CoA**. - Succinyl-CoA can be converted into **oxaloacetate** and then to glucose via gluconeogenesis, but it does not produce ketone bodies. *Arginine* - Arginine is a purely **glucogenic** amino acid, serving as a precursor for **α-ketoglutarate** in the TCA cycle. - This pathway allows its carbon skeleton to be diverted into glucose production, but it does not yield ketone bodies.

Question 10: Which of the following binds to Tyrosine Kinase receptor?

A. Insulin (Correct Answer)
B. Glucagon
C. Prolactin
D. Growth Hormone

Explanation: ***Insulin*** - **Insulin** is a classic example of a hormone that binds to and activates a **tyrosine kinase receptor**, leading to a cascade of intracellular signaling events for glucose uptake and metabolism. - The **insulin receptor** is a heterodimeric protein with intrinsic tyrosine kinase activity that phosphorylates itself and other proteins upon insulin binding. *Glucagon* - **Glucagon** primarily acts on **G protein-coupled receptors (GPCRs)**, specifically the glucagon receptor, to increase cyclic AMP (cAMP) and activate protein kinase A. - Its main roles are to stimulate **glycogenolysis** and **gluconeogenesis** in the liver. *Prolactin* - **Prolactin** binds to a receptor that is a member of the **cytokine receptor superfamily**, which lacks intrinsic enzyme activity. - Upon ligand binding, these receptors associate with and activate **Janus kinases (JAKs)**, leading to the JAK-STAT signaling pathway. *Growth Hormone* - **Growth hormone (GH)** also binds to a receptor belonging to the **cytokine receptor superfamily** (similar to prolactin), which then associates with and activates **JAKs**. - This activation subsequently initiates the **JAK-STAT signaling pathway**, mediating its diverse growth-promoting and metabolic effects.

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