Molecular Cloning and Chromosomal Localization of the MouseGpr37Gene Encoding an Orphan G-Protein-Coupled Peptide Receptor Expressed in Brain and Testis

Marazziti, D.; Gallo, Angela; Golini, Elisabetta; Matteoni, Rafaele; Tocchini‐Valentini, Glauco P.

doi:10.1006/geno.1998.5433

Cited by 55 publications

(57 citation statements)

References 42 publications

(57 reference statements)

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“…GPR37 is predominantly expressed in the mouse brain and testis (Zeng et al 1997, Marazziti et al 1998. A recent report found that its purified ligand is neuropeptide head activator (HA; Rezgaoui et al 2006).…”

Section: Discussionmentioning

confidence: 99%

G-protein-coupled receptors in aldosterone-producing adenomas: a potential cause of hyperaldosteronism

Ye¹,

Mariniello²,

Mantero³

et al. 2007

Journal of Endocrinology

105

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The source of aldosterone in 30-40% of patients with primary hyperaldosteronism (PA) is unilateral aldosterone-producing adenoma (APA). The mechanisms causing elevated aldosterone production in APA are unknown. Herein, we examined the expression of G-protein-coupled receptors (GPCRs) in APA and demonstrated that when compared with normal adrenals, there is a general elevation of certain GPCR in many APA and/or ectopic expression of GPCR in others. RNA samples from normal adrenals (nZ5), APAs (nZ10), and cortisol-producing adenomas (CPAs; nZ13) were used on 15 genomic expression arrays, each of which included 223 GPCR transcripts presented in at least 1 out of 15 of the independent microarrays. The array results were confirmed using real-time RT-PCR (qPCR). Four GPCR transcripts exhibited a statistically significant increase that was greater than threefold when compared with normal adrenals, suggesting a general increase in expression when compared with normal adrenal glands. Four GPCR transcripts exhibited a O15-fold increase of expression in one or more of the APA samples when compared with normal adrenals. qPCR analysis confirmed array data and found the receptors with the highest fold increase in APA expression to be LH receptor, serotonin receptor 4, GnRH receptor, glutamate receptor metabotropic 3, endothelin receptor type B-like protein, and ACTH receptor. There are also sporadic increased expressions of these genes in the CPAs. Together, these findings suggest a potential role of altered GPCR expression in many cases of PA and provide candidate GPCR for further study.

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Section: Discussionmentioning

confidence: 99%

G-protein-coupled receptors in aldosterone-producing adenomas: a potential cause of hyperaldosteronism

Ye¹,

Mariniello²,

Mantero³

et al. 2007

Journal of Endocrinology

105

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“…5439168 (Gpr37l1<tm1.1Gtva>) and 5439169 (Gpr37l1<tm1.2Gtva>)]. G-protein-coupled receptors for the endothelin and bombesin peptides (17,20,21). Recently, the secreted neuro-and glioprotective glycoprotein prosaposin and derived peptides have been shown in vitro to interact with and activate both putative receptors (22).…”

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confidence: 99%

Precocious cerebellum development and improved motor functions in mice lacking the astrocyte cilium-, patched 1-associated Gpr37l1 receptor

Marazziti

Pietro

Golini

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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In the developing cerebellum, the proliferation and differentiation of glial and neuronal cell types depend on the modulation of the sonic hedgehog (Shh) signaling pathway. The vertebrate Gprotein-coupled receptor 37-like 1 (GPR37L1) gene encodes a putative G-protein-coupled receptor that is expressed in newborn and adult cerebellar Bergmann glia astrocytes. This study shows that the ablation of the murine Gpr37l1 gene results in premature down-regulation of proliferation of granule neuron precursors and precocious maturation of Bergmann glia and Purkinje neurons. These alterations are accompanied by improved adult motor learning and coordination. Gpr37l1 −/− mice also exhibit specific modifications of the Shh signaling cascade. Specific assays show that in Bergmann glia cells Gpr37l1 is associated with primary cilium membranes and it specifically interacts and colocalizes with the Shh primary receptor, patched 1. These findings indicate that the patched 1-associated Gpr37l1 receptor participates in the regulation of postnatal cerebellum development by modulating the Shh pathway.mutant mouse model | mitogenic signaling

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“…G protein-coupled receptor ͉ Parkinson's disease ͉ dopamine transporter T he orphan G protein-coupled receptor 37 (GPR37) is homologous to endothelin (ET B -R) and bombesin (GRP-R, NMB-R) receptors (1) and it is highly expressed in mammalian brain oligodendrocytes, Purkinje cells, and neurons belonging to the CA3 hippocampal region and to the substantia nigra (SN) pars compacta (2). GPR37 is a substrate of the ubiquitin-protein ligase parkin, and it has been named parkin-associated endothelin-like receptor (PAEL-R) (3).…”

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confidence: 99%

GPR37 associates with the dopamine transporter to modulate dopamine uptake and behavioral responses to dopaminergic drugs

Marazziti

Mandillo

Pietro

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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106

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The orphan G protein-coupled receptor 37 (GPR37) is a substrate of parkin; its insoluble aggregates accumulate in brain samples of Parkinson's disease patients. We report here that GPR37 interacts with the dopamine transporter (DAT) and modulates DAT activity. GPR37 and DAT were found colocalized in mouse striatal presynaptic membranes and in transfected cells and their interaction was confirmed by coimmunoprecipitation assays. Gpr37-null mutant mice showed enhanced DAT-mediated dopamine uptake in striatal membrane samples, with a significant increase in the number of plasma membrane DAT molecules. The null mutant mice also exhibited a decrease in cocaine-induced locomotor activity and in catalepsy induced by dopamine receptor antagonists. These results reveal the specific role of GPR37, a putative peptidergic G proteincoupled receptor, in modulating the functional expression of DAT and the behavioral responses to dopaminergic drugs.G protein-coupled receptor ͉ Parkinson's disease ͉ dopamine transporter T he orphan G protein-coupled receptor 37 (GPR37) is homologous to endothelin (ET B -R) and bombesin (GRP-R, NMB-R) receptors (1) and it is highly expressed in mammalian brain oligodendrocytes, Purkinje cells, and neurons belonging to the CA3 hippocampal region and to the substantia nigra (SN) pars compacta (2). GPR37 is a substrate of the ubiquitin-protein ligase parkin, and it has been named parkin-associated endothelin-like receptor (PAEL-R) (3). An insoluble form of GPR37 is accumulated in brain samples of Parkinson's disease (PD) patients, and the overexpression of GPR37 in cell cultures, in the absence of parkin, can lead to unfolded protein-induced cell death (3, 4). Little is known about the physiological function of the receptor in the brain and in dopaminergic neurons in particular, although it has been speculated that the aggregation of GPR37 in insoluble complexes is responsible for the preferential loss of SN neurons through the endoplasmic reticulum-specific apoptotic pathway (5, 6). Recent data reported an interaction between GPR37, the head activator neuropeptide and its binding protein (sorting protein-related receptor; SorLA), supporting the hypothesis that GPR37 is involved in neuronal cell survival (7). To investigate the receptor's function, we generated homozygous Gpr37-null mutant mice, which exhibit a reduction in striatal dopamine (DA) content, specific locomotor deficits, and enhanced sensitivity to amphetamine (8).Several binding partners for the DA transporter (DAT) have been identified, suggesting that a regulated multiprotein complex controls its synthesis, targeting, and expression at specific cellular membrane domains (9). Presynaptic DAT expression is of crucial importance in modulating the synaptic availability of DA at nigrostriatal synapses, and its regulation is dynamically controlled for the maintenance of normal dopaminergic neurotransmission. The increase or decrease of DAT expression in the presynaptic membranes results in decreased or increased synaptic DA concentration, ...

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Molecular Cloning and Chromosomal Localization of the MouseGpr37Gene Encoding an Orphan G-Protein-Coupled Peptide Receptor Expressed in Brain and Testis

Cited by 55 publications

References 42 publications

G-protein-coupled receptors in aldosterone-producing adenomas: a potential cause of hyperaldosteronism

G-protein-coupled receptors in aldosterone-producing adenomas: a potential cause of hyperaldosteronism

Precocious cerebellum development and improved motor functions in mice lacking the astrocyte cilium-, patched 1-associated Gpr37l1 receptor

GPR37 associates with the dopamine transporter to modulate dopamine uptake and behavioral responses to dopaminergic drugs

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