GPR132 Membrane Protein Introduction

Introduction of GPR132

GPR132 is encoded by the GPR132 gene, and the protein is also termed as G2A. It was originally identified as an orphan G protein-coupled receptor (GPCR) induced by DNA damage and stress. There are two alternative splice variants, G2A-a and G2A-b. The seven-pass transmembrane receptor can actively modulate several cellular biological activities, such as cell cycle, proliferation, and immunity. The third α-helix play important role in the maintenance of protein stability and receptor activation.

Basic Information of GPR132
Protein Name G-protein coupled receptor 132
Gene Name GPR132
Aliases G2A
Organism Homo sapiens (Human)
UniProt ID Q9UNW8
Transmembrane Times 7
Length (aa) 380

Function of GPR132 Membrane Protein

As a pH-sensing receptor, GPR132 resides in the cell surface membrane to sense changes in extracellular pH, contributing to mediate the reciprocal interaction between cancer cells and macrophages. So GPR132 can regulate cancer cell metastasis and proliferation, immune cell function, inflammation and blood vessel formation. Gpr132 was demonstrated to be a target for activation by Foxp1, a transcription factor that plays key roles in normal lymphopoiesis and lymphoid malignancies. The interaction of Foxp1 and GPR132 may cause cell cycle changes, including G2 arrest. The regulatory function identifies GPR132 as a potential new therapeutic target for cancer treatment and chemoprevention. Furthermore, GPR132, predominantly expressed in the hematopoietic tissues and macrophages, cannot only mediate immune cell migration and phagocytosis but also regulate auto-immunity and lymphocyte homeostasis. The Gpr132 knockout mice exhibit abnormal expansion of both T and B lymphocytes, leading to a severe late-onset autoimmune syndrome. GPR132 was suggested to be a receptor for lysophosphatidylcholine (LPC) and fatty acid metabolites.

The regulatory mechanism of GPR132 in human breast cancer. Fig.1 The regulatory mechanism of GPR132 in human breast cancer. (Chen P, et al. 2017)

Application of GPR132 Membrane Protein in Literature

  1. Bond J., et al. Direct interaction of Ikaros and Foxp1 modulates expression of the G protein-coupled receptor G2A in B-lymphocytes and acute lymphoblastic leukemia. Oncotarget. 2016, 7(40): 65923. PubMed ID: 27588474

    This article identifies that Gpr132 is a novel target for Foxp1, and the interaction is realized by direct binding. Overexpression of Foxp1 in pre-B cells enhanced Gpr132 transcription and significantly affected the cell cycle, including G2 arrest. Binding of Foxp1 to the Gpr132 gene is inhibited by wild-type Ikaros, a transcription factor influencing the lymphopoiesis and lymphoid malignancies. In Ikaros-deleted acute lymphoblastic leukemia, GPR132 is evaluated as a potential modulator of the cell cycle.

  2. Cohen L.J., et al. Functional metagenomic discovery of bacterial effectors in the human microbiome and isolation of commendamide, a GPCR G2A/132 agonist. Proceedings of the National Academy of Sciences. 2015, 112(35): E4825- E4834. PubMed ID: 26283367

    The authors isolate a small molecular N-acyl-3-hydroxyglycines, which can structurally mimic host signaling metabolites. N-acyl-3-hydroxyglycines can activate GPR132/G2A, potentially involved in autoimmune disease and atherosclerosis.

  3. Chen P., et al. Gpr132 sensing of lactate mediates tumor–macrophage interplay to promote breast cancer metastasis. Proceedings of the National Academy of Sciences. 2017, 114(3): 580-585. PubMed ID: 28049847

    This article highlights that GPR132 can sense the rising lactate in the acidic tumor milieu, which mediates the reciprocal interaction between cancer cells and macrophages during breast cancer metastasis. Activated by lactate, GPR132 promotes the alternative activation of macrophage (M2)-like phenotype, facilitating cancer cell adhesion, migration, and invasion. The deletion of Gpr132 can inverse this bioprocess.

  4. Hohmann S.W., et al. The G2A receptor (GPR132) contributes to oxaliplatin-induced mechanical pain hypersensitivity. Scientific Reports. 2017, 7(1): 446. PubMed ID: 28348394

    This article reports the involvement of GPR132 in oxaliplatin induced neuropathic pain in mice. The G2A-receptor knockout mice showed lower mechanical hypersensitivity after oxaliplatin treatment. In the sciatic nerve and dorsal root ganglia of oxaliplatin-treatment mice, lipid ligands of G2A maintain high concentration.

  5. Justus C.R., et al. Acidic tumor microenvironment and pH-sensing G protein-coupled receptors. Frontiers in physiology. 2013, 4: 354. PubMed ID: 24367336

    The authors summarize that GPR132 participates in the regulation of cancer cell metastasis and proliferation, inflammation, and blood vessel formation. Activated by acidosis, the proton-sensing GPCRs can transduce multiple downstream G protein signaling pathways.

GPR132 Preparation Options

To obtain the soluble and functional target protein, the versatile Magic™ membrane protein production platform in Creative Biolabs enables many flexible options, from which you can always find a better match for your particular project. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-GPR132 antibody development services.

Creative Biolabs is world widely approved of the rich experience to prepare the membrane protein, a technical difficulty in protein engineering. Numerous challenging projects choose us based on our advanced research, strong technical force, and highly cooperative group. Using various strategies, we can provide professional preparation services to help the customer get the desired membrane protein. Please feel free to contact us for more information.

Online Inquiry

Verification code
Click image to refresh the verification code.


USA: 45-1 Ramsey Road, Shirley, NY 11967, USA
Europe: Heidenkampsweg 58, 20097 Hamburg, Germany
Call us at:
USA: 1-631-381-2994
Europe: 44-207-097-1828
Fax: 1-631-207-8356
Our customer service representatives are available 24 hours a day, 7 days a week. Contact Us