Target intelligence / Profile preview

Regulator of G-protein signaling 7 (RGS7)

Target
RGS7
Molecular classification
GTPase-activating protein (GAP), Signal transduction regulator, RGS protein (Regulator of G protein signaling)
01

Overview

Regulator of G-protein signaling 7 (RGS7) is a member of the R7 subfamily of RGS proteins, highly expressed in the nervous system and periphery[2][3]. RGS7 functions as a GTPase-activating protein (GAP), accelerating the deactivation of heterotrimeric G proteins and hence attenuating GPCR signaling. It forms multisubunit complexes (particularly with Gβ5 and R7BP) required for precise spatial and temporal control of GPCR pathways involved in neurotransmission, vision, learning, memory, and metabolic regulation[1][2]. RGS7 interacts with several family members, unique orphan GPCRs (GPR158, GPR179), and anchoring proteins (R7BP, R9AP), affecting its cellular localization and activity[1][2]. Disruption of RGS7 function is linked to neuropsychiatric diseases, cancer, and diabetes, and the RGS7 complex is under investigation as a drug target to improve the efficacy and safety of GPCR-modulating therapies[1].

Other names
RGS7Regulator of G protein signaling 7regulator of G-protein signaling RGS7regulator of G-protein signalling 7Regulator of G-protein signaling 7, RGS7regulator of G protein signaling 7
02

Mechanism of action

Drugs targeting RGS7 would act by inhibiting or enhancing its GAP activity, thus prolonging or reducing GPCR signaling. Potential mechanisms include allosteric modulation of RGS7-Gβ5 complex formation and stabilization or disruption of RGS7 interactions with protein partners (such as R7BP, GPR158, GPR179).

03

Biological functions

Signal transductionRegulation of GPCR-mediated neurotransmissionModulation of synaptic transmissionControl of vision, memory, learningRegulation of insulin secretion
04

Disease associations

Neuropsychiatric disease (e.g., drug addiction, learning/memory deficits)Cancer progressionMetabolic disorders, including diabetes (via insulin modulation)
05

Safety considerations

Therapeutic modulation of RGS7 may risk off-target effects due to its widespread expression and regulatory role in multiple essential GPCR pathways.Potential impact on cognition, addiction vulnerability, insulin regulation, and neuronal excitability.
06

Interacting drugs

No approved drugs directly target RGS7 as of 2024.

2 more in the full profile.

07

Biomarkers

Currently, there are no clinically validated biomarkers for RGS7 patient selection or monitoring.Altered expression in brain or pancreatic tissues is experimentally associated with susceptibility to neuropsychiatric and metabolic disorders.

Beyond the preview

Go deeper on Regulator of G-protein signaling 7 (RGS7).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Regulator of G-protein signaling 7 (RGS7).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call