Signal Transduction Practice Questions

Q: cGMP acts as second messenger for ?

Nitric oxide. ***Nitric oxide*** - **Nitric oxide (NO)** activates **guanylyl cyclase**, which then converts GTP to **cGMP**. - **cGMP** mediates many of NO's biological effects, including **vasodilation**. *Dopamine* - **Dopamine** primarily acts through **G-protein coupled receptors** that affect adenylate cyclase activity, leading to changes in **cAMP** levels, not cGMP. - Its effects are often mediated by changes in neuronal excitability and neurotransmission. *Calcitonin* - **Calcitonin** is a hormone that primarily acts to lower **blood calcium levels**. - Its receptors are typically coupled to **G-proteins** that activate **adenylate cyclase** to produce **cAMP**. *FSH* - **Follicle-stimulating hormone (FSH)** binds to receptors on target cells in the gonads. - This binding generally activates **adenylate cyclase**, leading to the production of **cAMP**, which acts as a second messenger.

Q: Which of these hormones activate catalytic receptors?

IGF1. ***Correct: IGF1*** - **IGF-1** binds to the **IGF-1 receptor (IGF-1R)**, which is a **receptor tyrosine kinase (RTK)** with **intrinsic catalytic activity** [1]. - Upon IGF-1 binding, the receptor undergoes **autophosphorylation** and directly phosphorylates intracellular substrates through its own tyrosine kinase domain [2]. - This qualifies as a **true catalytic receptor** because the enzymatic activity is intrinsic to the receptor itself [3]. *Incorrect: Leptin* - Leptin binds to the **leptin receptor (Ob-R)**, which is a member of the **cytokine receptor family**. - This receptor **lacks intrinsic enzymatic activity** and instead signals through **associated Janus kinases (JAKs)** via the JAK-STAT pathway. - Since the catalytic activity comes from associated proteins (JAKs) rather than the receptor itself, this is **not classified as a catalytic receptor**. *Incorrect: GH* - **Growth Hormone (GH)** binds to the **GH receptor**, another member of the cytokine receptor superfamily. - Like the leptin receptor, the GH receptor **does not have intrinsic catalytic activity** but relies on associated JAKs for signal transduction via the JAK-STAT pathway. - This is **not a catalytic receptor** because the enzymatic function is provided by associated kinases, not the receptor itself. **Key Distinction:** - **Catalytic receptors** = Receptors with intrinsic enzymatic activity (e.g., receptor tyrosine kinases, receptor serine/threonine kinases) [1], [3] - **Cytokine receptors** = Receptors that recruit associated kinases but lack intrinsic catalytic domains

Q: Which of the following hormones stimulates the production of cAMP?

Calcitonin. ***Calcitonin*** - Calcitonin binds to its receptor, which is a **G-protein coupled receptor (GPCR)**, stimulating **adenylyl cyclase**. - This activation of adenylyl cyclase leads to the production of **cyclic AMP (cAMP)** from ATP, which then acts as a second messenger. *Somatostatin* - Somatostatin typically binds to **Gi-protein-coupled receptors**, which **inhibit adenylyl cyclase** activity. - This action leads to a **decrease in cAMP production**, thereby reducing the release of various hormones. *Acetylcholine* - Acetylcholine can act through both **nicotinic** and **muscarinic receptors**. Muscarinic receptors are GPCRs. - While some muscarinic receptors can inhibit adenylyl cyclase (M2, M4), others primarily activate **phospholipase C**, leading to increased **IP3 and DAG** rather than cAMP. *Angiotensin II* - Angiotensin II primarily acts through **GPCRs (AT1 and AT2 receptors)**, predominantly activating the **phospholipase C pathway**. - This results in the production of **inositol triphosphate (IP3)** and **diacylglycerol (DAG)**, which increase intracellular calcium, rather than stimulating cAMP production.

Q: All are true regarding G protein Except?

Active conformation has all three subunits. ***Active conformation has all three subunits*** - The **active conformation** of a G protein typically involves the dissociation of the **alpha subunit** from the **beta-gamma dimer** upon GTP binding. - The alpha subunit, now bound to GTP, and the beta-gamma dimer then activate downstream effector proteins independently; thus, the fully trimeric structure is not the active conformation. *It has a trimeric structure* - In its **inactive state**, a G protein is indeed a **heterotrimer** composed of alpha (α), beta (β), and gamma (γ) subunits, with GDP bound to the alpha subunit. - This **trimeric structure** is a defining characteristic of G proteins before activation by a G protein-coupled receptor. *Alpha subunit has GTPase activity* - The alpha subunit of a G protein possesses intrinsic **GTPase activity**, which is crucial for terminating signaling. - This activity allows it to **hydrolyze bound GTP back to GDP**, returning the G protein to its inactive state. *It is activated by GTP binding* - G proteins are activated when a **guanosine diphosphate (GDP)** molecule bound to the alpha subunit is exchanged for a **guanosine triphosphate (GTP)** molecule. - This **GTP binding** is triggered by the activation of a G protein-coupled receptor (GPCR) by its ligand, leading to conformational changes that facilitate nucleotide exchange.

Q: If there is a Gs alpha subunit gain-of-function mutation, this results in

Increased cAMP. ***Increased cAMP*** - A **gain-of-function mutation** in the **Gs alpha subunit** means it remains in its active, GTP-bound state for longer. - The activated Gs alpha subunit stimulates **adenylyl cyclase**, leading to persistently high levels of **cAMP**. *Decreased cAMP* - This would result from a **loss-of-function** mutation in the Gs alpha subunit or a gain-of-function in an inhibitory G protein (Gi), not a Gs gain-of-function. - A decrease in cAMP would inhibit downstream signaling pathways, which is the opposite of what occurs with Gs activation. *Increased GTPase activity* - **GTPase activity** is responsible for hydrolyzing GTP to GDP, which inactivates the G alpha subunit. - A gain-of-function mutation often implies **reduced GTPase activity**, causing the G protein to stay active longer, not increased activity. *Decreased IP* - **IP3 (inositol trisphosphate)** is a secondary messenger produced via the activation of **phospholipase C**, typically by Gq proteins. - Gs alpha subunit mutations primarily affect the **adenylyl cyclase/cAMP pathway**, not the inositol phosphate pathway.

Q: JAK-STAT kinase receptors are associated with?

Nuclear transcription. ***Nuclear transcription*** - JAK-STAT signaling is a **ligand-activated pathway** that directly regulates gene transcription in response to cytokines and growth factors. - Upon activation, **STAT proteins** translocate to the nucleus to act as transcription factors, modulating gene expression. *Ion channels* - **Ion channels** are transmembrane proteins that allow the passage of ions across cell membranes, typically involved in electrical signaling. - Their activity is usually regulated by **voltage changes** or direct ligand binding, not primarily by JAK-STAT signaling. *IP3 - DAG* - The **inositol triphosphate (IP3)** and **diacylglycerol (DAG)** pathway is a second messenger system primarily activated by G protein-coupled receptors (GPCRs). - This pathway leads to intracellular **calcium release** and protein kinase C activation, distinct from JAK-STAT. *cAMP* - **cAMP** (cyclic adenosine monophosphate) is a common second messenger activated by GPCRs, leading to the activation of **protein kinase A (PKA)**. - This signaling cascade is distinct from the direct transcriptional role of the JAK-STAT pathway.

Q: Which of the following act through tyrosine kinase receptor:

Insulin. ***Insulin*** - **Insulin** binds to its specific receptor, which is a **tyrosine kinase receptor**, leading to autophosphorylation and activation of downstream signaling pathways. - This activation results in glucose uptake, metabolism, and storage in target cells. *GH* - **Growth Hormone (GH)** primarily acts through **JAK/STAT signaling pathways** after binding to its receptor, which is a cytokine receptor, not a direct tyrosine kinase receptor. - The GH receptor itself does not possess intrinsic tyrosine kinase activity but rather recruits and activates associated kinases. *FSH* - **Follicle-stimulating hormone (FSH)** mediates its effects by binding to a **G protein-coupled receptor (GPCR)** on target cells. - Activation of the **GPCR** leads to the generation of **cAMP** as a second messenger, which then modulates cellular processes. *Glucagon* - **Glucagon** also acts through a **G protein-coupled receptor (GPCR)** on liver cells. - Binding of glucagon to its receptor activates **adenylyl cyclase**, leading to an increase in **cAMP** levels and subsequently increased glycogenolysis and gluconeogenesis.

Q: In the mitogen activated protein kinase pathway, the activation of RAS is counteracted by

GTPase activating protein. ***GTPase activating protein*** - **GTPase Activating Proteins (GAPs)** facilitate the hydrolysis of **GTP bound to RAS** to GDP, converting active RAS back to its inactive state. - This inactivation is crucial for turning off the downstream signaling of the **MAPK pathway** and preventing uncontrolled cell proliferation. *Inositol triphosphate* - **Inositol triphosphate (IP3)** is a secondary messenger that triggers the release of **intracellular calcium** from the endoplasmic reticulum. - It is involved in various signaling pathways, but its primary role is not to directly counteract RAS activation. *Phosphatidyl inositol* - **Phosphatidylinositol (PI)** is a component of cell membranes and can be phosphorylated to produce various **phosphatidylinositol phosphates (PIPs)**, like **PIP2** and **PIP3**. - These molecules act as docking sites for signaling proteins but do not directly inactivate RAS. *Protein kinase C* - **Protein kinase C (PKC)** is a family of enzymes involved in signal transduction, typically activated by **diacylglycerol (DAG)** and calcium. - It phosphorylates various proteins, mediating diverse cellular responses, but it does not directly counteract the activation of RAS.

Q: Pertussis toxin acts by all of the following mechanisms except ?

Increased calcium release from sarcoplasmic reticulum. ***Increased calcium release from sarcoplasmic reticulum*** - Pertussis toxin does NOT directly cause increased calcium release from the sarcoplasmic reticulum. - While increased cAMP can have downstream effects on calcium signaling, **direct calcium release from SR is not a characteristic mechanism** of pertussis toxin action. - This is the exception among the listed mechanisms. *Acts through G alpha subunit* - Pertussis toxin primarily acts by **ADP-ribosylating** the αi subunit of **G proteins** (Gαi), effectively inhibiting its function. - This inhibition leads to the **inactivation of Gi proteins**, preventing them from inhibiting adenylate cyclase. - This is the PRIMARY mechanism of pertussis toxin. *Increase cyclic AMP* - The inhibition of Gi proteins by pertussis toxin leads to **constitutive activation of adenylate cyclase**. - This results in a **sustained increase in intracellular cyclic AMP (cAMP)** levels. - This is a well-established consequence of pertussis toxin action. *ADP ribosylation of proteins associated with receptors* - Pertussis toxin specifically acts as an **ADP-ribosyltransferase**, transferring an ADP-ribose group from NAD+ to target proteins. - This modification occurs on the **alpha-inhibitory subunit (Giα)** of heterotrimeric G proteins, which are associated with various cell surface receptors. - This is the molecular mechanism by which pertussis toxin exerts its effects.

Q: Which set of hormones exclusively utilizes nuclear receptors?

Vitamin D, Retinoic acid, Progesterone. ***Vitamin D, Retinoic acid, Progesterone*** - **Vitamin D**, **retinoic acid**, and **progesterone** are all **lipid-soluble molecules** that can readily cross the cell membrane and bind to **intracellular nuclear receptors**. - Their binding to nuclear receptors directly influences **gene transcription** and protein synthesis. *Estrogen, Thyroxine, Insulin* - While **estrogen** and **thyroxine** utilize nuclear receptors, **insulin** is a peptide hormone that binds to **cell surface receptors**. - **Insulin** activates a signal transduction cascade, rather than directly influencing gene transcription via nuclear receptors. *Cortisol, Aldosterone, TSH* - **Cortisol** and **aldosterone** are steroid hormones that bind to nuclear receptors. - However, **TSH (Thyroid Stimulating Hormone)** is a peptide hormone that binds to **G protein-coupled receptors** on the cell surface of thyroid cells. *Progesterone, Testosterone, Glucagon* - **Progesterone** and **testosterone** are steroid hormones that utilize nuclear receptors. - **Glucagon** is a peptide hormone that binds to **G protein-coupled receptors** on the cell surface of target cells, primarily hepatocytes.

Question 1

cGMP acts as second messenger for ?

Accepted Answer

Nitric oxide

Answer

Dopamine

Answer

Calcitonin

Answer

FSH

Question 2

Which of these hormones activate catalytic receptors?

Accepted Answer

IGF1

Answer

All of these

Answer

Leptin

Answer

GH

Question 3

Which of the following hormones stimulates the production of cAMP?

Accepted Answer

Calcitonin

Answer

Somatostatin

Answer

Acetylcholine

Answer

Angiotensin II

Question 4

All are true regarding G protein Except?

Accepted Answer

Active conformation has all three subunits

Answer

It has a trimeric structure

Answer

Alpha subunit has GTPase activity

Answer

It is activated by GTP binding

Question 5

If there is a Gs alpha subunit gain-of-function mutation, this results in

Accepted Answer

Increased cAMP

Answer

Decreased cAMP

Answer

Increased GTPase activity

Answer

Decreased IP₃

Question 6

JAK-STAT kinase receptors are associated with?

Accepted Answer

Nuclear transcription

Answer

Ion channels

Answer

IP3 - DAG

Answer

cAMP

Question 7

Which of the following act through tyrosine kinase receptor:

Accepted Answer

Insulin

Answer

GH

Answer

FSH

Answer

Glucagon

Question 8

In the mitogen activated protein kinase pathway, the activation of RAS is counteracted by

Accepted Answer

GTPase activating protein

Answer

Inositol triphosphate

Answer

Phosphatidyl inositol

Answer

Protein kinase C

Question 9

Pertussis toxin acts by all of the following mechanisms except ?

Accepted Answer

Increased calcium release from sarcoplasmic reticulum

Answer

Increase cyclic AMP

Answer

Acts through G alpha subunit

Answer

ADP ribosylation of proteins associated with receptors

Question 10

Which set of hormones exclusively utilizes nuclear receptors?

Accepted Answer

Vitamin D, Retinoic acid, Progesterone

Answer

Estrogen, Thyroxine, Insulin

Answer

Cortisol, Aldosterone, TSH

Answer

Progesterone, Testosterone, Glucagon

Signal Transduction — MCQs

Signal Transduction — MCQs

On this page

Practice by Chapter

Want unlimited practice?