Signal Transduction — MCQs

Signal Transduction Indian Medical PG Practice Questions and MCQs

Question 121: What does cAMP activate?

A. Protein kinase 'A' (Correct Answer)
B. Protein kinase 'C'
C. Nuclear transcription
D. Phospholipase

Explanation: ***Protein kinase 'A'*** - **cAMP** (cyclic adenosine monophosphate) acts as a **second messenger** that directly binds to and activates **protein kinase A (PKA)**. - The activation of PKA leads to the phosphorylation of various downstream target proteins, mediating a wide range of cellular responses. *Protein kinase 'C'* - **Protein kinase C (PKC)** is primarily activated by **diacylglycerol (DAG)** and **calcium ions**, not cAMP. - PKC is involved in different signaling pathways, often initiated by Gq protein-coupled receptors. *Nuclear transcription* - While cAMP signaling and PKA activation can ultimately influence **gene expression** in the nucleus, cAMP does not directly activate nuclear transcription itself. - Instead, PKA phosphorylates **transcription factors** that then regulate gene expression. *Phospholipase* - **Phospholipase** enzymes, such as **phospholipase C**, are typically responsible for generating second messengers like **diacylglycerol (DAG)** and **inositol triphosphate (IP3)** from membrane phospholipids. - They are upstream of other signaling cascades and are not directly activated by cAMP.

Question 122: In apoptosis, protein hydrolysis is due to activation of

A. Caspases (Correct Answer)
B. Lipases
C. Transcarboxylase
D. Catalase

Explanation: ***Caspases*** - **Caspases** are a family of **cysteine proteases** that play essential roles in apoptosis by cleaving specific protein substrates. - Their activation initiates a cascade of proteolytic events leading to the organized dismantling of the cell during programmed cell death. *Lipases* - **Lipases** are enzymes that specifically hydrolyze **ester bonds in lipids** (fats). - They are primarily involved in fat digestion and metabolism, not the protein hydrolysis characteristic of apoptosis. *Transcarboxylase* - **Transcarboxylase** is an enzyme involved in the transfer of a **carboxyl group** during metabolic reactions, particularly in the synthesis of fatty acids. - It does not play a direct role in the proteolytic degradation of proteins during apoptosis. *Catalase* - **Catalase** is an enzyme that catalyzes the decomposition of **hydrogen peroxide into water and oxygen**. - It functions in protecting cells from oxidative damage, and not in protein hydrolysis during apoptosis.

Question 123: Which hormone is a derivative of Proopiomelanocortin (POMC)?

A. Acetylcholine
B. Adrenocorticotropic hormone (ACTH) (Correct Answer)
C. Dopamine
D. Norepinephrine

Explanation: ***Adrenocorticotropic hormone (ACTH)*** - **Proopiomelanocortin (POMC)** is a large precursor polypeptide that is cleaved into several active peptide hormones, including **ACTH**. - This processing occurs in different tissues, producing various biologically active peptides from a single gene product. *Dopamine* - **Dopamine** is a **neurotransmitter** and **hormone** derived from the amino acid **tyrosine**. - It is not a direct cleavage product of the POMC polypeptide. *Acetylcholine* - **Acetylcholine** is a **neurotransmitter** synthesized from **choline** and **acetyl-CoA**. - It is not related to the POMC precursor protein. *Norepinephrine* - **Norepinephrine** (also known as **noradrenaline**) is a **catecholamine** derived from **dopamine** and, ultimately, from the amino acid **tyrosine**. - It is not a derivative of the POMC precursor.

Question 124: Nitric oxide acts by increasing which of the following?

A. BRCA 1
B. BRCA 2
C. Interleukin
D. cGMP (Correct Answer)

Explanation: ***cGMP*** - **Nitric oxide (NO)** activates **guanylyl cyclase**, which then converts **GTP** to **cyclic guanosine monophosphate (cGMP)** - **cGMP** is a secondary messenger that mediates many of NO's biological effects, including **vasodilation** through the activation of **protein kinase G (PKG)** - This is the primary mechanism of action of nitric oxide in various physiological processes *BRCA 1* - **BRCA1** is a **tumor suppressor gene** involved in **DNA repair**, not directly increased by nitric oxide - Mutations in **BRCA1** are associated with an increased risk of **breast** and **ovarian cancers** - No direct relationship with nitric oxide signaling pathway *BRCA 2* - Similar to BRCA1, **BRCA2** is a **tumor suppressor gene** crucial for **DNA repair** and genomic stability - **Nitric oxide** does not directly increase the levels or activity of **BRCA2** - Functions independently of NO signaling *Interleukin* - **Interleukins** are a group of **cytokines** that play a crucial role in the **immune response**, inflammation, and cell communication - While nitric oxide can modulate immune responses that involve interleukins, it does not directly increase **interleukin** levels as its primary signaling mechanism - The relationship is indirect and not the primary action of NO

Question 125: Which of the following statements is true regarding the functions of cAMP and cGMP?

A. All of the above statements are true
B. They act on membrane receptors.
C. They are both second messengers. (Correct Answer)
D. They act by post-translational modification.

Explanation: ***They are both second messengers.*** - **cAMP (cyclic adenosine monophosphate)** and **cGMP (cyclic guanosine monophosphate)** are crucial intracellular signaling molecules. - They relay signals from **first messengers** (like hormones or neurotransmitters) received at the cell surface to intracellular targets, thus acting as second messengers. *They act on membrane receptors.* - **cAMP** and **cGMP** are *produced* in response to activation of **membrane receptors** by first messengers, but they themselves do not act directly on these receptors. - Their action is primarily *intracellular*, binding to and activating various enzymes and proteins like **protein kinases**. *All of the above statements are true* - This statement is incorrect because the claim that they act on membrane receptors is false. - Only one of the statements provided is accurate regarding the functions of cAMP and cGMP. *They act by post-translational modification.* - While cAMP and cGMP can lead to **post-translational modification** (e.g., phosphorylation by protein kinases A and G), they are not themselves the direct modifiers. - They act as **allosteric regulators** of enzymes, which then catalyze the modifications.

Question 126: Tyrosine kinase receptor is associated with proto-oncogene -

A. RAS (RAt Sarcoma)
B. RET (REarranged during Transfection) (Correct Answer)
C. RB (Retinoblastoma gene)
D. MYC (Myelocytomatosis oncogene)

Explanation: ***RET*** - RET is a **tyrosine kinase receptor** that plays a crucial role in cell signaling and development [1][2]. - It is associated with several **neoplasms**, including medullary thyroid carcinoma and multiple endocrine neoplasia type 2 [1]. *RB* - RB (Retinoblastoma protein) is a **tumor suppressor gene**, not a proto-oncogene or receptor. - Its role is largely in regulating the **cell cycle**, particularly in preventing excessive cell growth. *RAS* - RAS is a family of **GTPase proteins** involved in transmitting signals within cells, but it is not a receptor itself [1]. - It is classified as an **oncogene**, but does not function as a tyrosine kinase receptor [2]. *MYC* - MYC is a **transcription factor** involved in cell cycle progression and growth, not a tyrosine kinase receptor [2]. - It is considered an **oncogene** that promotes cellular proliferation, but it doesn't have tyrosine kinase activity [3][4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1097-1098. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 291-292. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 28-29. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 293-294.

Question 127: Which of the following statements are true regarding the visual cycle cascade?

A. All of the options are true (Correct Answer)
B. Light causes isomerization of 11-cis-retinal to all-trans-retinal
C. Retinal is involved in the visual cycle
D. Involves a conformational change in opsin

Explanation: ***All of the statements are true*** The visual cycle cascade involves multiple interconnected events in phototransduction: **Light causes isomerization of 11-cis-retinal to all-trans-retinal** - This is the **primary photochemical event** that initiates vision - Light absorption causes the **cis-trans isomerization** in less than a picosecond - This conformational change is the only light-dependent step in the entire cascade **Retinal is involved in the visual cycle** - **11-cis-retinal** serves as the chromophore bound to opsin forming rhodopsin - After isomerization to **all-trans-retinal**, it must be converted back to 11-cis-retinal - This regeneration occurs through the **retinoid cycle** involving RPE cells **Involves a conformational change in opsin** - The isomerization of retinal triggers **conformational changes in opsin** - This converts rhodopsin to **metarhodopsin II** (the active form) - Activated opsin then activates **transducin** (G-protein), amplifying the signal and leading to hyperpolarization of photoreceptor cells All three statements accurately describe essential components of the visual cycle cascade.

Question 128: 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 129: Glucagon activates which enzyme ?

A. Adenylyl cyclase (Correct Answer)
B. Pepsin
C. Trypsin
D. None of the options

Explanation: ***Adenylyl cyclase*** - **Glucagon** binds to specific G protein-coupled receptors on target cells, activating the **Gαs subunit**. - The activated **Gαs subunit** then stimulates **adenylyl cyclase**, leading to the production of **cyclic AMP (cAMP)**, which mediates glucagon's metabolic effects. *Pepsin* - **Pepsin** is a protease produced in the stomach, involved in protein digestion, and its activity is regulated by **gastrin** and **acid secretion**, not glucagon. - It is synthesized as **pepsinogen** and activated by hydrochloric acid (HCl) at low pH. *Trypsin* - **Trypsin** is a digestive enzyme produced in the pancreas and secreted into the small intestine, primarily involved in protein digestion. - Its activation is dependent on **enteropeptidase**, which cleaves **trypsinogen**, and its activity is not directly regulated by glucagon. *None of the options* - This option is incorrect because **adenylyl cyclase** is indeed activated by glucagon as part of its signaling pathway.

Question 130: What is the role of Anandamide in the human body?

A. Opioid
B. D2 blocker
C. Cannabinoid neurotransmitter (Correct Answer)
D. CCK1 antagonist

Explanation: ***Cannabinoid neurotransmitter*** - **Anandamide** is an **endogenous cannabinoid neurotransmitter** that binds to **CB1** and **CB2 receptors**. - It plays a role in **pain modulation**, **appetite stimulation**, and **memory regulation**. *Opioid* - **Opioids** bind to **opioid receptors** (mu, delta, kappa) and are known for their **analgesic** and **euphoric effects**. - Examples include **morphine** and **endorphins**, which are chemically distinct from anandamide and have different receptor targets. *CK 1 antagonist* - This option refers to a **cholecystokinin 1 (CCK1) receptor antagonist**, which would block the effects of **CCK**. - **CCK** is a hormone involved in **digestion** and **satiety**, and its role is unrelated to anandamide. *D2 blocker* - A **D2 blocker** is an agent that antagonizes the **dopamine D2 receptor**. - These are typically **antipsychotic medications** that modulate **dopamine pathways** in the brain, unrelated to the function of anandamide.

Practice by Chapter

Cell Surface Receptors: Types and Functions

Practice Questions

G-Protein Coupled Receptors

Practice Questions

Enzyme-Linked Receptors

Practice Questions

Second Messengers in Signal Transduction

Practice Questions

cAMP and cGMP Signaling

Practice Questions

Calcium as Second Messenger

Practice Questions

Inositol Phosphate Pathway

Practice Questions

MAP Kinase Cascades

Practice Questions

JAK-STAT Signaling Pathway

Practice Questions

Insulin Signaling Pathway

Practice Questions

Nuclear Receptors and Gene Regulation

Practice Questions

Defects in Signal Transduction and Disease

Practice Questions

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