In which conditions is cAMP produced? #1 B -arrestin is always active. #2 Lack of kinase domain in BARK #3 ß1-adrenergic membrane receptor lacking it’s ligand-binding domain

Human Anatomy & Physiology (11th Edition)
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Chapter1: The Human Body: An Orientation
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In which conditions is cAMP produced? #1 B -arrestin is always active. #2 Lack of kinase domain in BARK #3 ß1-adrenergic membrane receptor lacking it’s ligand-binding domain
**Title: Mechanism of Adrenaline Action via β1-Adrenergic Receptor**

This diagram illustrates the cellular signaling pathway activated by adrenaline through the β1-adrenergic receptor, leading to physiological effects such as increased heart rate and fat breakdown.

**Pathway Description:**

- **Adrenaline Binding:**
  - Adrenaline, depicted as small triangles outside the cell, binds to the β1-adrenergic receptor located on the plasma membrane.

- **Receptor Activation:**
  - This binding activates the receptor, which initiates a cascade of intracellular events.

- **G Protein Activation:**
  - The receptor activates a G protein by facilitating the exchange of GDP for GTP on the G protein. 

- **Adenylyl Cyclase Activation:**
  - The activated G protein, associated with GTP, in turn activates adenylyl cyclase.

- **cAMP Production:**
  - Adenylyl cyclase catalyzes the conversion of ATP to cyclic AMP (cAMP).

- **Protein Kinase A Activation:**
  - cAMP then activates Protein Kinase A (PKA).

- **Physiological Effects:**
  - Activated PKA leads to increased fat breakdown and an increased heart rate through phosphorylation of specific target proteins.

- **Regulatory Mechanisms:**
  - β-arrestin mediates receptor desensitization and alters signaling pathways to prevent overstimulation.
  - BARK (β-adrenergic receptor kinase) also contributes to receptor regulation.

**Diagram Notations:**
- Solid arrows represent activation steps in the signaling pathway.
- T-bar symbols indicate repression mechanisms.

This pathway exemplifies how adrenaline influences metabolic and cardiac functions, highlighting the intricate regulation within cellular signaling networks.
Transcribed Image Text:**Title: Mechanism of Adrenaline Action via β1-Adrenergic Receptor** This diagram illustrates the cellular signaling pathway activated by adrenaline through the β1-adrenergic receptor, leading to physiological effects such as increased heart rate and fat breakdown. **Pathway Description:** - **Adrenaline Binding:** - Adrenaline, depicted as small triangles outside the cell, binds to the β1-adrenergic receptor located on the plasma membrane. - **Receptor Activation:** - This binding activates the receptor, which initiates a cascade of intracellular events. - **G Protein Activation:** - The receptor activates a G protein by facilitating the exchange of GDP for GTP on the G protein. - **Adenylyl Cyclase Activation:** - The activated G protein, associated with GTP, in turn activates adenylyl cyclase. - **cAMP Production:** - Adenylyl cyclase catalyzes the conversion of ATP to cyclic AMP (cAMP). - **Protein Kinase A Activation:** - cAMP then activates Protein Kinase A (PKA). - **Physiological Effects:** - Activated PKA leads to increased fat breakdown and an increased heart rate through phosphorylation of specific target proteins. - **Regulatory Mechanisms:** - β-arrestin mediates receptor desensitization and alters signaling pathways to prevent overstimulation. - BARK (β-adrenergic receptor kinase) also contributes to receptor regulation. **Diagram Notations:** - Solid arrows represent activation steps in the signaling pathway. - T-bar symbols indicate repression mechanisms. This pathway exemplifies how adrenaline influences metabolic and cardiac functions, highlighting the intricate regulation within cellular signaling networks.
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