Characterization of a naturally-occurring polymorphism in the UHR-1 gene encoding the putative rat prolactin-releasing peptide receptor

Kate L J Ellacott; Emma L. Donald; Paul Clarkson; John Morten; Dave Masters; John Brennand; Simon M. Luckman

doi:10.1016/j.peptides.2004.11.020

Characterization of a naturally-occurring polymorphism in the UHR-1 gene encoding the putative rat prolactin-releasing peptide receptor

Kate L J Ellacott, Emma L. Donald, Paul Clarkson, John Morten, Dave Masters, John Brennand, Simon M. Luckman

Research output: Contribution to journal › Article › peer-review

Abstract

The rat orphan receptor UHR-1 and its human orthologue, GPR10, were first isolated in 1995. The ligand for this receptor, prolactin-releasing peptide (PrRP), was identified in 1998 by reverse pharmacology and has subsequently been implicated in a number of physiological processes. As supported by its localization and regulation in the hypothalamus and brainstem, we have shown previously that PrRP is involved in energy homeostasis. Here we describe a naturally occurring polymorphism in the UHR-1 gene that results in an ATG to ATA change at the putative translational initiation site. The presence of the polymorphism abolished the binding of 125I PrRP in rat brain slices but did not affect the ability of PrRP to reduce fast-induced food intake. Together this data suggest that PrRP may be exerting its feeding effects through a receptor other than UHR-1. © 2004 Elsevier Inc. All rights reserved.

Original language	English
Pages (from-to)	675-681
Number of pages	6
Journal	Peptides
Volume	26
Issue number	4
DOIs	https://doi.org/10.1016/j.peptides.2004.11.020
Publication status	Published - Apr 2005

Keywords

Food intake
Genetic variation
PrRP
Receptor autoradiography
UHR-1

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10.1016/j.peptides.2004.11.020

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title = "Characterization of a naturally-occurring polymorphism in the UHR-1 gene encoding the putative rat prolactin-releasing peptide receptor",

abstract = "The rat orphan receptor UHR-1 and its human orthologue, GPR10, were first isolated in 1995. The ligand for this receptor, prolactin-releasing peptide (PrRP), was identified in 1998 by reverse pharmacology and has subsequently been implicated in a number of physiological processes. As supported by its localization and regulation in the hypothalamus and brainstem, we have shown previously that PrRP is involved in energy homeostasis. Here we describe a naturally occurring polymorphism in the UHR-1 gene that results in an ATG to ATA change at the putative translational initiation site. The presence of the polymorphism abolished the binding of 125I PrRP in rat brain slices but did not affect the ability of PrRP to reduce fast-induced food intake. Together this data suggest that PrRP may be exerting its feeding effects through a receptor other than UHR-1. {\textcopyright} 2004 Elsevier Inc. All rights reserved.",

keywords = "Food intake, Genetic variation, PrRP, Receptor autoradiography, UHR-1",

author = "Ellacott, {Kate L J} and Donald, {Emma L.} and Paul Clarkson and John Morten and Dave Masters and John Brennand and Luckman, {Simon M.}",

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T1 - Characterization of a naturally-occurring polymorphism in the UHR-1 gene encoding the putative rat prolactin-releasing peptide receptor

AU - Ellacott, Kate L J

AU - Donald, Emma L.

AU - Clarkson, Paul

AU - Morten, John

AU - Masters, Dave

AU - Brennand, John

AU - Luckman, Simon M.

PY - 2005/4

Y1 - 2005/4

N2 - The rat orphan receptor UHR-1 and its human orthologue, GPR10, were first isolated in 1995. The ligand for this receptor, prolactin-releasing peptide (PrRP), was identified in 1998 by reverse pharmacology and has subsequently been implicated in a number of physiological processes. As supported by its localization and regulation in the hypothalamus and brainstem, we have shown previously that PrRP is involved in energy homeostasis. Here we describe a naturally occurring polymorphism in the UHR-1 gene that results in an ATG to ATA change at the putative translational initiation site. The presence of the polymorphism abolished the binding of 125I PrRP in rat brain slices but did not affect the ability of PrRP to reduce fast-induced food intake. Together this data suggest that PrRP may be exerting its feeding effects through a receptor other than UHR-1. © 2004 Elsevier Inc. All rights reserved.

AB - The rat orphan receptor UHR-1 and its human orthologue, GPR10, were first isolated in 1995. The ligand for this receptor, prolactin-releasing peptide (PrRP), was identified in 1998 by reverse pharmacology and has subsequently been implicated in a number of physiological processes. As supported by its localization and regulation in the hypothalamus and brainstem, we have shown previously that PrRP is involved in energy homeostasis. Here we describe a naturally occurring polymorphism in the UHR-1 gene that results in an ATG to ATA change at the putative translational initiation site. The presence of the polymorphism abolished the binding of 125I PrRP in rat brain slices but did not affect the ability of PrRP to reduce fast-induced food intake. Together this data suggest that PrRP may be exerting its feeding effects through a receptor other than UHR-1. © 2004 Elsevier Inc. All rights reserved.

KW - Food intake

KW - Genetic variation

KW - PrRP

KW - Receptor autoradiography

KW - UHR-1

U2 - 10.1016/j.peptides.2004.11.020

DO - 10.1016/j.peptides.2004.11.020

M3 - Article

SN - 1873-5169

VL - 26

SP - 675

EP - 681

JO - Peptides

JF - Peptides

IS - 4

ER -

Characterization of a naturally-occurring polymorphism in the UHR-1 gene encoding the putative rat prolactin-releasing peptide receptor

Abstract

Keywords

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