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Neuropeptide B/W GPCR Assays

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Background of Neuropeptide B/W Receptors

Neuropeptide B/W receptors (NPBWRs) have recently been classified in the G-protein coupled receptor superfamily with an affinity for Neuropeptide B/W peptides. There are two subtypes of NPBWRs which are identified as NPBWR-1 and NPBWR-2. These two receptors are essential in aspects of mood regulation, control of circadian rhythms, and diet control, they also greatly affect neuroendocrine regulation and pain perception.

Structure of the Human Neuropeptide B/W receptor 1.Fig.1. Structure of the Human Neuropeptide B/W receptor 1. (Uniprot ID P48145; obtained from Alphafold)

Distribution and Function of Neuropeptide B/W Receptors

The distribution of NPBWRs varies in different species. Only the presence of NPBWR1 can be determined in rodents, in contrast, both of the NPBWRs can be found in humans and other mammals. NPBWRs are widely distributed in the nervous system and some of the vital organs. NPBWRs can work as an efficient target in modulating the pituitary-derived hormone releasement, manipulating the sleep-wake cycle, and pain control.

Subtypes and Mechanisms of Neuropeptide B/W Receptors

Two members of neuropeptide B/W receptors have been successfully cloned, NPBWR1 and NPBWR2.

Receptor Gene Mechanism Agonists Antagonists

NPBWR1

GPR7

  • NPBWR1 binds to NPW and NPB
  • NPFFR1 functionally couples to Gi and affects cAMP production.
  • Neuropeptide W
  • Neuropeptide B
  • CTM 50769

NPBWR2

GPR8

  • NPBWR2 binds to NPW and NPB.
  • NPBWR2 functionally couples to Gi and affects cAMP production.
  • Neuropeptide W
  • Neuropeptide B

Assay List of Neuropeptide B/W Receptors

Creative Biolabs can provide a range of assays of neuropeptide B/W receptors. You can choose the assay in the list or contact us for more information:

NPBWR1 NPBWR2
Assay No. Assay Name Host Cell Assay Type Datasheet
Calcium Flux Assay
S01YF-1122-KX667 Magic™ Human NPBWR1 In Vitro Calcium Flux Assay CHO-K1 Calcium Flux Assay
S01YF-1122-KX671 Magic™ Mouse NPBWR1 In Vitro Calcium Flux Assay CHO-K1 Calcium Flux Assay
S01YF-1122-KX672 Magic™ Rat NPBWR1 In Vitro Calcium Flux Assay CHO-K1 Calcium Flux Assay
[35S]GTPγS Binding Assay
S01YF-1122-KX669 Magic™ Human NPBWR1 In Vitro [35S]GTPγS binding Assay CHO-K1 [35S]GTPγS binding Assay
Radioligand Binding Assay
S01YF-1122-KX670 Magic™ Human NPBWR1 In Vitro Radioligand Binding Assay CHO-K1 Radioligand Binding Assay
Assay No. Assay Name Host Cell Assay Type Datasheet
Calcium Flux Assay
S01YF-1122-KX673 Magic™ Human NPBWR2 In Vitro Calcium Flux Assay CHO-K1 Calcium Flux Assay
[35S]GTPγS Binding Assay
S01YF-1122-KX675 Magic™ Human NPBWR2 In Vitro [35S]GTPγS binding Assay CHO-K1 [35S]GTPγS binding Assay
Radioligand Binding Assay
S01YF-1122-KX676 Magic™ Human NPBWR2 In Vitro Radioligand Binding Assay CHO-K1 Radioligand Binding Assay

Published Data

Paper Title

Neuropeptide B and neuropeptide W as new serum predictors of nutritional status and of clinical outcomes in pediatric patients with type 1 diabetes mellitus treated with the use of pens or insulin pumps

Journal

Archives of Medical Science

Published

2019

Abstract The pathogenesis of type 1 diabetes mellitus (T1DM) involves changes in the central nervous system, autoimmune mechanisms, fat and bone tissue, and a large number of biomolecules are involved in these processes. Previous studies have demonstrated that in the CNS, neuropeptide B/W and its receptors can directly participate in the regulation of energy homeostasis and play a role in the pathogenesis and outcome of T1DM. Leptin influences pro-inflammatory cytokines, and controls the AMP activation process and insulin secretion. Adiponectin controls appetite, regulates energy, affects glucose and lipid metabolism, and participates in insulin response in T1DM patients. Experiments also proved the influence of nuclear factor ligand and osteocalcin in the process of T1DM. The purpose of this study was to evaluate the relationship between the levels of NPB/W and its receptors, adiponectin, SRANKL, leptin, and other key molecules in individual children with T1DM and clinical treatment. The researchers hypothesized that different methods of insulin administration would lead to correlated changes in the molecular levels in the serum of pediatric T1DM patients, and that responses would be produced through regulatory pathways in the central nervous system, adipose tissue, and bone, thus demonstrating the effect of insulin administration on glycemic control and the crosstalk between bone-derived molecules, adipokines, and neuropeptides.
Result The experiment recruited 58 T1DM patients and 25 healthy controls. Under different insulin administration methods (insulin pen or continuous hypodermic injection device), NPB, NPW, leptin, osteocalcin, adiponectin, sRANKL, and total antioxidant status (TAS) were analyzed. Data showed that TAS, leptin, and NPB/W contents were relatively low in T1DM patients, adiponectin levels also varied, free sRANKL and osteocalcin contents were similar to those in the control group. In addition, insulin dosing assays showed that study parameters other than NPW were not directly related to the degree of glycemic control. Experimental results showed that serum levels of leptin, adiponectin, TAS, and NPB/W were altered in pediatric patients with T1DM, and these biomolecules and neuropeptides regulate carbohydrate metabolism and energy cycling in diabetic patients. This study identified the clinical relationship between neuropeptides, adipose, and bone-derived factors with T1DM, suggesting that molecules such as NPW/B and leptin could be used as potential diagnostic indicators in children and adolescents with T1DM.

Characteristic curves of serum levels of test factors.Fig.2. Characteristic curves of serum levels of test factors. (Grzelak, 2019)

Reference

  1. Grzelak, T.; et al. Neuropeptide B and neuropeptide W as new serum predictors of nutritional status and of clinical outcomes in pediatric patients with type 1 diabetes mellitus treated with the use of pens or insulin pumps. Archives of Medical Science. 2019, 15(3): 619-631.
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