Neuropeptide receptors / Ivone Gomes ... [and others].

Format:

Book

Contributor:

Gomes, Ivone.

Series:

Colloquium digital library of life sciences

Colloquium series on neuropeptides ; 2166-6636 # 4.

Colloquium series on neuropeptides, 2166-6636 ; # 4

Language:

English

Subjects (All):

Neuropeptides--Receptors.

Neuropeptides.

Receptors, Neuropeptide.

Medical Subjects:

Receptors, Neuropeptide.

Physical Description:

1 online resource (xiv, 153 pages) : illustrations.

Place of Publication:

San Rafael, Calif. (1537 Fourth Street, San Rafael, CA 94901 USA) : Morgan & Claypool, [2013]

System Details:

Mode of access: World Wide Web.

text file

Summary:

Neuropeptides mediate their effects by binding and activating receptors that are responsible for converting these extracellular stimuli into intracellular responses. Most neuropeptides interact with G protein-coupled receptors that transduce the signal by activating heterotrimeric G proteins leading to alterations in second messenger systems to amplify the signal and elicit the intracellular response. In this review, we describe the general structure of G protein-coupled receptors including the information obtained from crystal structure determination that has given an insight into the activation mechanism of these receptors. In addition, we summarize the components of the signal transduction system (including G proteins, effectors and second messengers generally activated by the neuropeptide receptors). Using select examples of neuropeptide-receptor systems, we highlight the neuropeptides and corresponding receptors involved in modulation of pain and analgesia, body weight regulation, and hormonal regulation. Finally, we discuss the enzyme-linked tyrosine kinase receptors activated by growth factors and discuss the emerging concepts in targeting neuropeptide receptors for the identification of novel therapeutics targeting these systems.

Contents:

1. Overview of neuropeptide receptors

2. G protein-coupled receptors: general structure & function

2.1 Introduction

2.2 Topology and classification of G protein-coupled receptors

2.2.1 Class A GPCRS

2.2.2 Class B GPCRS

2.2.3 Class C GPCRS

2.3 Conformational and structural changes associated with receptor activation

2.3.1 The crystal structure of CXCR4 receptor

2.3.2 The crystal structure of the [mu] opioid receptor

2.3.3 The crystal structure of the [kappa] opioid receptor

2.3.4 The crystal structure of the [delta] opioid receptor

2.3.5 The crystal structure of the nociceptin/orphanin FQ receptor

2.4 Domains involved in GPCR dimerization/heteromerization

3. G protein-coupled receptor signaling

3.1 Introduction

3.2 G protein-mediated signaling

3.2.1 The G[alpha]s family

3.2.2 The G[alpha]i/o family

3.2.3 The G[alpha]q/11 family

3.2.4 The G[beta-gamma] family

3.3 Direct effectors of G protein-mediated signaling

3.3.1 Adenylyl cyclases

3.3.2 Phospholipases

3.3.3 G protein-gated inwardly rectifying K+ channels

3.3.4 Voltage-gated CA2+ channels

3.4 Downstream effectors of G protein-mediated signaling

3.4.1 Cyclic AMP

3.4.2 Calcium and phosphoinositides

3.5 GPCR desensitization and down-regulation

3.5.1 G protein-coupled receptor kinases

3.5.2 [Beta]-arrestins

3.6 G protein-independent signaling

3.7 [Beta]-arrestin-dependent signaling and biased agonism

3.8 Modulation of GPCR signaling by heterodimerization

4. Neuropeptide processing and regulation

4.1 Introduction

4.2 Neuropeptide processing

4.3 Neuropeptide sorting

4.4 Neuropeptide secretion

4.5 Neuropeptide degradation

5. Neuropeptide receptors

5.1 Introduction

5.2 Neuropeptides and their receptors

5.3 Enzyme-linked receptors

5.4 Peripherally synthesized proteins/peptides and their receptors in the brain

6. Perspectives

References.

Notes:

Part of: Colloquium digital library of life sciences.

Title from PDF t.p. (viewed on June 17, 2013).

Series from website.

Includes bibliographical references (pages 93-153).

Other Format:

Print version:

ISBN:

9781615044696

Access Restriction:

Restricted for use by site license.