Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

GPCR Desensitization01:12

GPCR Desensitization

6.2K
G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
6.2K
Transducer Mechanism: G Protein–Coupled Receptors01:30

Transducer Mechanism: G Protein–Coupled Receptors

9.1K
G Protein–Coupled Receptors (GPCRs) are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to various stimuli. GPCRs regulate critical physiological pathways and are excellent drug targets for treating diseases such as diabetes, cancer, obesity, depression, or Alzheimer's. Nearly 35% of approved drugs implement their therapeutic effects by selectively interacting with specific GPCRs.
GPCRs are also called heptahelical,...
9.1K
G Protein-coupled Receptors01:15

G Protein-coupled Receptors

14.2K
G Protein-Coupled Receptors or GPCRs are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to sensory stimuli such as light, odors, hormones, cytokines, or neurotransmitters.
GPCRs are also called heptahelical, 7TM, or serpentine receptors, and consist of seven (H1-H7) transmembrane alpha-helices that span the bilayer to form a cylindrical core. The transmembrane helices are connected by three extracellular loops and three...
14.2K
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

6.9K
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
6.9K
G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

5.5K
GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory...
5.5K
G-protein Coupled Receptors01:21

G-protein Coupled Receptors

92.3K
G-protein coupled receptors are ligand binding receptors that indirectly affect changes in the cell. The actual receptor is a single polypeptide that transverses the cell membrane seven times creating intracellular and extracellular loops. The extracellular loops create a ligand specific pocket which binds to neurotransmitters or hormones. The intracellular loops holds onto the G-protein.
92.3K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Visual arrestin-1: how did we learn what we know today about this protein?

Progress in retinal and eye research·2026
Same author

Arrestin-3 promotes locomotor sensitization to psychostimulants via JNK signaling in nucleus accumbens.

bioRxiv : the preprint server for biology·2026
Same author

GRKs and arrestins: Nomenclature and functions in GPCR-dependent and -independent signalling.

British journal of pharmacology·2026
Same author

Arrestin-3 sca-olds multiple MAP3Ks driving stress-induced JNK3 activation and cell death.

bioRxiv : the preprint server for biology·2026
Same author

Cytoplasmic tail diversity determines the effector bias of the adhesion GPCR ADGRL2.

Cell chemical biology·2026
Same author

Deceptive beauty of non-natural structures.

Protein science : a publication of the Protein Society·2026

Related Experiment Video

Updated: May 5, 2026

Monitoring GPCR-β-arrestin1/2 Interactions in Real Time Living Systems to Accelerate Drug Discovery
08:21

Monitoring GPCR-β-arrestin1/2 Interactions in Real Time Living Systems to Accelerate Drug Discovery

Published on: June 28, 2019

6.2K

Targeting individual GPCRs with redesigned nonvisual arrestins.

Luis E Gimenez1, Sergey A Vishnivetskiy, Vsevolod V Gurevich

  • 1Department of Pharmacology, Vanderbilt University, 2200 Pierce Avenue, Nashville, TN, 37232, USA, luis.e.gimenez@vanderbilt.edu.

Handbook of Experimental Pharmacology
|December 3, 2013
PubMed
Summary
This summary is machine-generated.

Enhanced arrestins can improve visual system function by quenching overactive G protein-coupled receptors (GPCRs). This research paves the way for developing targeted therapies for diseases caused by GPCR signaling imbalances.

More Related Videos

Parallel Interrogation of β-Arrestin2 Recruitment for Ligand Screening on a GPCR-Wide Scale using PRESTO-Tango Assay
09:03

Parallel Interrogation of β-Arrestin2 Recruitment for Ligand Screening on a GPCR-Wide Scale using PRESTO-Tango Assay

Published on: March 10, 2020

11.9K
Optimizing the Genetic Incorporation of Chemical Probes into GPCRs for Photo-crosslinking Mapping and Bioorthogonal Chemistry in Live Mammalian Cells
14:02

Optimizing the Genetic Incorporation of Chemical Probes into GPCRs for Photo-crosslinking Mapping and Bioorthogonal Chemistry in Live Mammalian Cells

Published on: April 9, 2018

7.9K

Related Experiment Videos

Last Updated: May 5, 2026

Monitoring GPCR-β-arrestin1/2 Interactions in Real Time Living Systems to Accelerate Drug Discovery
08:21

Monitoring GPCR-β-arrestin1/2 Interactions in Real Time Living Systems to Accelerate Drug Discovery

Published on: June 28, 2019

6.2K
Parallel Interrogation of β-Arrestin2 Recruitment for Ligand Screening on a GPCR-Wide Scale using PRESTO-Tango Assay
09:03

Parallel Interrogation of β-Arrestin2 Recruitment for Ligand Screening on a GPCR-Wide Scale using PRESTO-Tango Assay

Published on: March 10, 2020

11.9K
Optimizing the Genetic Incorporation of Chemical Probes into GPCRs for Photo-crosslinking Mapping and Bioorthogonal Chemistry in Live Mammalian Cells
14:02

Optimizing the Genetic Incorporation of Chemical Probes into GPCRs for Photo-crosslinking Mapping and Bioorthogonal Chemistry in Live Mammalian Cells

Published on: April 9, 2018

7.9K

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Human diseases often stem from dysregulated signaling of G protein-coupled receptors (GPCRs).
  • Arrestins are key regulators of GPCR signaling, and their functional compensation is being explored as a therapeutic strategy.
  • Previous studies tested enhanced arrestins in the visual system, showing improvements in rod photoreceptor function.

Purpose of the Study:

  • To investigate the therapeutic potential of enhanced arrestins in dampening hyperactive GPCR signaling.
  • To assess the feasibility of developing receptor subtype-specific nonvisual arrestins for therapeutic applications.

Main Methods:

  • Construction of structurally distinct enhanced arrestin mutants with higher affinity for active GPCRs.
  • Testing the efficacy of these "super-arrestins" in a demanding visual system model.
  • Identifying key arrestin residues responsible for receptor discrimination.

Main Results:

  • Enhanced arrestins improved rod morphology, light sensitivity, survival, and photoresponse recovery in the visual system.
  • Structurally distinct enhanced arrestin mutants demonstrated higher affinity for active GPCRs.
  • Identification of specific arrestin residues crucial for receptor subtype specificity.

Conclusions:

  • Enhanced arrestins show promise in mitigating signaling from hyperactive GPCRs.
  • Developing receptor subtype-specific nonvisual arrestins is a viable strategy for targeted therapeutic interventions.
  • This research opens avenues for novel treatments for GPCR-related human diseases.