Cloning of GPR37, a Gene Located on Chromosome 7 Encoding a Putative G-Protein-Coupled Peptide Receptor, from a Human Frontal Brain EST Library

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

doi:10.1006/geno.1997.4900

Cited by 60 publications

(77 citation statements)

References 46 publications

(7 reference statements)

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“…Gpr37 Ϫ/Ϫ mice showed a reduced cataleptic response to the administration of each antagonist (SCH23390: F (1,15) ϭ 11.43, P Ͻ 0.005; haloperidol: F (1,18) ϭ 3.88, P ϭ 0.06). The difference between genotypes in the time spent in a cataleptic posture after the injection of both drugs was dose-dependent (SCH23390: F (3,45) ϭ 306.88, P Ͻ 0.001; haloperidol: F (3,54) ϭ 27.76, P Ͻ 0.001). Additionally, the repeated-measures ANOVA revealed a significant effect of the interaction genotype ϫ dose of both drugs (SCH23390: F (3,45) ϭ 11.49, P Ͻ 0.001; haloperidol: F (3,54) ϭ 3.66, P Ͻ 0.05).…”

Section: Reduced Catalepsy By D1 and D2 Receptor Antagonists In Gpr37mentioning

confidence: 98%

“…The difference between genotypes in the time spent in a cataleptic posture after the injection of both drugs was dose-dependent (SCH23390: F (3,45) ϭ 306.88, P Ͻ 0.001; haloperidol: F (3,54) ϭ 27.76, P Ͻ 0.001). Additionally, the repeated-measures ANOVA revealed a significant effect of the interaction genotype ϫ dose of both drugs (SCH23390: F (3,45) ϭ 11.49, P Ͻ 0.001; haloperidol: F (3,54) ϭ 3.66, P Ͻ 0.05). The Gpr37 Ϫ/Ϫ mice showed a significantly reduced cataleptic response at the dose of 0.1 mg/kg SCH23390 and 0.5 mg/kg haloperidol (Fig.…”

Section: Reduced Catalepsy By D1 and D2 Receptor Antagonists In Gpr37mentioning

confidence: 98%

“…HEK293 cells and HEK-hDAT cells were maintained in Dulbecco's modified Eagle's medium with 10% FBS, 2 mM Lglutamine, 100 units/ml penicillin, and 100 g/ml streptomycin; 400 g/ml geneticin (G418) was added only to HEK-hDAT cells. Full-length human GPR37 cDNA containing an HA peptide tag at its carboxyl terminus (GPR37-HA) was obtained from total human brain RNA (45) and cloned in the pcDNA3 expression vector (Invitrogen, Carlsbad, CA). The linearized GPR37-HA construct or vector plasmid were transfected with LipofectAMINE 2000 Reagent (Invitrogen) into cells grown to 70-80% confluency.…”

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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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Section: Reduced Catalepsy By D1 and D2 Receptor Antagonists In Gpr37mentioning

confidence: 98%

Section: Reduced Catalepsy By D1 and D2 Receptor Antagonists In Gpr37mentioning

confidence: 98%

mentioning

confidence: 99%

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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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“…Two orphan receptors are part of this group: GPR37 and GPR37L1 (Marazziti et al, 2001). We focused our interest on GPR37 because of its prominent expression in neurons of the brain compared with a more glial location of GPR37L1 (Marazziti et al, 1997;Zeng et al, 1997). GPR37 has also been isolated and characterised as a substrate for the ubiquitin ligase parkin, hence its alternative name -parkin-associated endothelin-like receptor (Pael R) (Imai et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

The neuropeptide head activator is a high-affinity ligand for the orphan G-protein-coupled receptor GPR37

Rezgaoui

Süsens

Ignatov

et al. 2006

Journal of Cell Science

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The neuropeptide head activator (HA) is a mitogen for mammalian cell lines of neuronal or neuroendocrine origin. HA signalling is mediated by a G-protein-coupled receptor (GPCR). Orphan GPCRs with homology to peptide receptors were screened for HA interaction. Electrophysiological recordings in frog oocytes and in mammalian cell lines as well as Ca2+ mobilisation assays revealed nanomolar affinities of HA to GPR37. HA signal transduction through GPR37 was mediated by an inhibitory G protein and required Ca2+ influx through a channel of the transient receptor potential (TRP) family. It also required activation of Ca2+-dependent calmodulin kinase and phosphoinositide 3-kinase. Respective inhibitors blocked HA signalling and HA-induced mitosis in GPR37-expressing cells. HA treatment resulted in internalisation of GPR37. Overexpression of GPR37 led to aggregate formation, retention of the receptor in the cytoplasm and low survival rates of transfected cells, confirming the notion that misfolded GPR37 contributes to cell death, as observed in Parkinson's disease.

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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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Cloning of GPR37, a Gene Located on Chromosome 7 Encoding a Putative G-Protein-Coupled Peptide Receptor, from a Human Frontal Brain EST Library

Cited by 60 publications

References 46 publications

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

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

The neuropeptide head activator is a high-affinity ligand for the orphan G-protein-coupled receptor GPR37

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

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