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Related Concept Videos

Adrenergic Receptors: β Subtype01:26

Adrenergic Receptors: β Subtype

β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
Adrenergic Receptors (Adrenoceptors): Classification01:27

Adrenergic Receptors (Adrenoceptors): Classification

Adrenergic receptors, or adrenoceptors, respond to the autonomic neurotransmitter noradrenaline and other endogenous catecholamine agonists. They are classified into two main families, α and β, based on their pharmacological response and are further subdivided depending on their location, elicited response, and affinity to specific agonists or antagonists.
α-Adrenoceptors
α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors, which are found on postsynaptic...
Adrenergic Receptors: ɑ Subtype01:31

Adrenergic Receptors: ɑ Subtype

Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase C—inositol-1,4,5-trisphosphate...
Adrenergic Antagonists: Chemistry and Classification of β-Receptor Blockers01:25

Adrenergic Antagonists: Chemistry and Classification of β-Receptor Blockers

β-adrenergic antagonists, or β-blockers, modulate the sympathetic nervous system by targeting β-adrenoceptors and inhibiting catecholamine-mediated sympathetic responses. β-blockers differ in their adrenoceptor subtype affinity, lipophilicity, and α-blocking capabilities. The history of β-blocker development began with the prototype, dichloroisoprenaline, which exhibited partial agonist activity. As a result, propranolol was developed as a pure antagonist but nonselective agent, paving the way...
Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

Adrenergic Antagonists: ɑ and β-Receptor Blockers

Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is clinically...
Adrenergic Agonists: Chemistry and Structure-Activity Relationship01:16

Adrenergic Agonists: Chemistry and Structure-Activity Relationship

Adrenergic agonists' structure-activity relationship (SAR) determines their selectivity and efficacy. These agonists comprise a phenylethylamine moiety with an aromatic ring and an ethylamine side chain.
Aromatic ring substitutions: Substituting the aromatic ring with –OH groups at positions 3 and 4 yields catecholamines (e.g., epinephrine), which have a high affinity for adrenoceptors. Hydrogen bonding between –OH groups and receptors enhances adrenergic activity.
Separation of the aromatic...

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Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
12:03

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Published on: June 7, 2016

Engineering an ultra-thermostable β(1)-adrenoceptor.

Jennifer L Miller1, Christopher G Tate

  • 1MRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.

Journal of Molecular Biology
|September 13, 2011
PubMed
Summary

Further stabilizing G-protein-coupled receptors (GPCRs) enhances their structure determination. New mutations significantly increase the thermostability of the β(1)-adrenoceptor mutant, improving its utility in crystallography.

Area of Science:

  • Biochemistry
  • Structural Biology
  • Pharmacology

Background:

  • Conformational thermostabilisation is key for determining G-protein-coupled receptor (GPCR) structures.
  • Thermostable GPCR mutants facilitate crystallography by tolerating detergents and adopting single conformations.
  • The β(1)-adrenoceptor mutant (β(1)AR-m23) was the first thermostabilised receptor structure determined.

Purpose of the Study:

  • To further enhance the thermostability of the β(1)AR-m23 mutant.
  • To investigate the impact of additional mutations on receptor stability and properties.
  • To identify optimal strategies for GPCR thermostabilisation.

Main Methods:

  • Introduction of three specific mutations (I129V, D322K, Y343L) into β(1)AR-m23.
  • Evaluation of thermostability using differential scanning fluorimetry in various detergents.

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  • Assessment of pharmacological properties and stability in short-chain and denaturing detergents.

    • Main Results:

    • A triple mutant of β(1)AR-m23 exhibited a 31°C increase in thermostability compared to wild-type and a 13°C increase over the original mutant.
    • Engineered salt bridges and leucine scanning mutagenesis proved most effective for improving thermostability.
    • The enhanced mutant maintained pharmacological properties and showed increased stability in detergents like heptylthioglucoside and SDS.

    Conclusions:

    • Additional mutations can significantly enhance GPCR thermostability beyond initial stabilisation efforts.
    • Thermostable GPCR mutants are crucial tools for structural biology, enabling studies in various detergent conditions.
    • Optimised thermostabilisation strategies are vital for advancing GPCR structure determination and drug discovery.