Interaction of NPY compounds with the rat glucocorticoid-induced receptor (GIR) reveals similarity to the NPY–Y2 receptor

Sah, Renu; Parker, Steven L.; Sheriff, Sulaiman; Eaton, Katherine; Balasubramaniam, Ambikaipakan; Sallee, Floyd R.

doi:10.1016/j.peptides.2006.11.013

Cited by 32 publications

(32 citation statements)

References 31 publications

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“…One caveat to this conclusion is the lack of a demonstrable difference in the efficiency of Foxp3 acquisition by naïve T cells in vivo in the absence or presence of GPR83, whereas it was suggested by others that GPR83 may facilitate the acquisition of Foxp3 expression (12). Although we cannot exclude the possibility that under certain conditions GPR83 signaling may be absolutely necessary, our results suggest that in vivo endogenous GPR83 plays a redundant role in the induction of Foxp3 expression in peripheral T cells, perhaps due to signals provided by other receptors, such as neuropeptide Y receptor 2, able to compensate for GPR83 deficiency (21). Moreover, it is possible that the discrepancy between our results and those of the study by Buer and coauthors is due to the reliance of the latter on the overexpression of GPR83 in naïve Foxp3 Ϫ T cells, which normally express GPR83 at low levels in both resting and activated states.…”

Section: Discussioncontrasting

confidence: 56%

G Protein-Coupled Receptor 83 Is Dispensable for the Development and Function of Regulatory T Cells

Lu¹,

Gavin²,

Rasmussen³

et al. 2007

Molecular and Cellular Biology

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Global analyses of gene expression in regulatory T (Treg) cells, whose development is critically dependent upon the transcription factor Foxp3, have provided many clues as to the molecular mechanisms these cells employ to control immune responses and establish immune tolerance. Through these studies, G proteincoupled receptor 83 (GPR83) was found to be expressed at high levels in Treg-cell populations. However, its function remained unclear. Recently, it has been suggested that GPR83 is involved in the induction of Foxp3 expression in the peripheral nonregulatory Foxp3 ؊ CD4 T cells. To examine a role for GPR83 in Treg-cell biology, we generated and characterized GPR83-deficient mice. We have shown that GPR83 abolition does not result in measurable pathology or changes in the numbers or function of Foxp3 ؉ Treg cells. Furthermore, while in vitro analysis suggested a potential involvement of GPR83 in transforming growth factor ␤-dependent Foxp3 induction, there was no difference in the ability of nonregulatory GPR83-deficient and nondeficient Foxp3 ؊ T cells to acquire Foxp3 expression in vivo. Collectively, our results demonstrate that GPR83 is dispensable for Treg-cell development and function.

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Section: Discussioncontrasting

confidence: 56%

G Protein-Coupled Receptor 83 Is Dispensable for the Development and Function of Regulatory T Cells

Lu¹,

Gavin²,

Rasmussen³

et al. 2007

Molecular and Cellular Biology

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“…4, C and D); thus, the HA tag did not appear to affect binding. A study examining rGPR83 reported binding of NPY (23). However, we found that NPY at concentrations below 1 μM did not displace [ 125 I]Tyr-rPEN and exhibited only a small (~20%) and not significant (one-way ANOVA; P = 0.37, F 7,40 = 1.109) displacement with 10 μM NPY (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Although GPR83 is currently referred to as an “orphan” GPCR, indicating that its ligand has not been definitively established, a report in 2007 claimed that NPY was a ligand for this receptor (23). We found that radiolabeled PEN binding to GPR83 was not affected by NPY concentrations below 1 μM, although 10 μM NPY caused a partial, nonsignificant, displacement of PEN binding.…”

Section: Discussionmentioning

confidence: 99%

Identification of GPR83 as the receptor for the neuroendocrine peptide PEN

et al. 2016

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PEN is an abundant peptide in the brain that has been implicated in the regulation of feeding. We identified a receptor for PEN in mouse hypothalamus and Neuro2A cells. PEN bound to and activated GPR83, a G protein (heterotrimeric guanine nucleotide–binding protein)–coupled receptor (GPCR). Reduction of GPR83 expression in mouse brain and Neuro2A cells reduced PEN binding and signaling, consistent with GPR83 functioning as the major receptor for PEN. In some brain regions, GPR83 colocalized with GPR171, a GPCR that binds the neuropeptide bigLEN, another neuropeptide that is involved in feeding and is generated from the same precursor protein as is PEN. Coexpression of these two receptors in cell lines altered the signaling properties of each receptor, suggesting a functional interaction. Our data established PEN as a neuropeptide that binds GPR83 and suggested that these two ligand-receptor systems—PEN-GPR83 and bigLEN-GPR171—may be functionally coupled in the regulation of feeding.

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“…Molecular profiling showed that POA WSN express Y2 as well as the GPR83, an orphan receptor sharing homology to Y2 and found by one group to interact with NPY in vitro (Sah et al, 2007; Eberwine and Bartfai, 2011; Dubins et al, 2012). Interestingly, downregulation of GPR83 expression in the POA by shRNA was recently shown to reduce CBT (discussed below; Dubins et al, 2012).…”

Section: Hypothalamic Orexigenic and Anorexigenic Peptidesmentioning

confidence: 99%

Molecules affecting hypothalamic control of core body temperature in response to calorie intake

Bartfai¹,

Conti²

2012

Front. Gene.

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Core body temperature (CBT) and calorie intake are main components of energy homeostasis and two important regulators of health, longevity, and aging. In homeotherms, CBT can be influenced by calorie intake as food deprivation or calorie restriction (CR) lowers CBT whereas feeding has hyperthermic effects. The finding that in mice CBT prolonged lifespan independently of CR, suggested that the mechanisms modulating CBT may represent important regulators of aging. Here we summarize the current knowledge on the signaling molecules and their receptors that participate in the regulation of CBT responses to calorie intake. These include hypothalamic neuropeptides regulating feeding but also energy expenditure via modulation of thermogenesis. We also report studies indicating that nutrient signals can contribute to regulation of CBT by direct action on hypothalamic preoptic warm-sensitive neurons that in turn regulate adaptive thermogenesis and hence CBT. Finally, we show the role played by two orphans G protein-coupled receptor: GPR50 and GPR83, that were recently demonstrated to regulate temperature-dependent energy expenditure.

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Interaction of NPY compounds with the rat glucocorticoid-induced receptor (GIR) reveals similarity to the NPY–Y2 receptor

Cited by 32 publications

References 31 publications

G Protein-Coupled Receptor 83 Is Dispensable for the Development and Function of Regulatory T Cells

G Protein-Coupled Receptor 83 Is Dispensable for the Development and Function of Regulatory T Cells

Identification of GPR83 as the receptor for the neuroendocrine peptide PEN

Molecules affecting hypothalamic control of core body temperature in response to calorie intake

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