Ask about this productRelated genes to: NPFF2 antibody
- Gene:
- NPFFR2 NIH gene
- Name:
- neuropeptide FF receptor 2
- Previous symbol:
- GPR74
- Synonyms:
- NPFF2, NPGPR
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-30
- Date modifiied:
- 2016-10-05
Related products to: NPFF2 antibody
Related articles to: NPFF2 antibody
- Prolactin-releasing peptide (PrRP), an RF-amide neuropeptide, is now recognized as an important regulator of food intake and body weight. This review summarizes current knowledge regarding the physiological roles of PrRP, its receptors prolactin-releasing peptide receptor (PRLHR/GPR10) and neuropeptide FF receptor 2 (NPFFR2/GPR74), and the therapeutic potential of PrRP analogs in obesity treatment. Experimental studies using PrRP-, GPR10-, and NPFFR2-knockout mouse models have demonstrated that disruption of PrRP signaling markedly affects energy homeostasis. PrRP- and GPR10-deficient mice generally develop increased body weight, hyperphagia, adiposity and impaired glucose homeostasis, whereas NPFFR2-knockout models exhibit more complex, sex- and diet-dependent metabolic phenotypes. Moreover, the first characterization of double GPR10/NPFFR2 knockout mice revealed severe late-onset obesity accompanied by profound metabolic disturbances. Current evidence further suggests that, although GPR10 is the primary receptor for PrRP, several lipidized PrRP analogs exhibit increased affinity for NPFF receptors, particularly NPFFR2, and may also interact with additional receptor systems. Experimental studies further indicate that the anti-obesity effects of PrRP analogs are mediated through the coordinated action of GPR10 and NPFFR2 signaling pathways. Recent advances in the development of lipidized and stabilized PrRP analogs have demonstrated promising anti-obesity effects in preclinical mouse models. Several analogs have shown prolonged efficacy with limited weight regain following treatment withdrawal. Together, these findings identify the PrRP system as a promising target for the development of novel therapies for obesity and related metabolic disorders. - Source: PubMed
Publication date: 2026/07/30
Škrlová MagdalenaStrnadová VeronikaŽelezná BlankaMaletínská Lenka - Tumor Treating Fields (TTFields) and pulsed electric fields (PEF) have emerged as a fourth modality in oncological treatment, succeeding surgery, radiotherapy, and pharmacotherapy. However, the fundamental mechanisms through which physical electrical stress is precisely transduced into biochemical signals remain to be fully elucidated. By integrating molecular dynamics simulations, multi-omics profiling, and the latest clinical trial data, this review systematically explores how electric fields, functioning as physical signals, initiate intracellular transduction by inducing conformational kinetic changes in G protein-coupled receptors (GPCRs), such as NPFFR2. Furthermore, we discuss how the modulation of waveform parameters enables the precise programming of apoptosis and pyroptosis patterns, thereby inducing immunogenic cell death (ICD) and activating the cGAS-STING pathway. Additionally, proteomics-based insights are employed to reveal the mechanisms of electric-field-induced compensatory resistance, and the pivotal role of electric fields in remodeling the tumor immune microenvironment and reversing resistance to immune checkpoint inhibitors is discussed. This review aims to provide refined theoretical guidance for the clinical translation of the emerging field of the "electro-immunome". - Source: PubMed
Publication date: 2026/07/09
Shi WeiZhao MengyaMa XiaofengDong LiSun Yulong - Neuropeptide FF receptor 2 (NPFFR2) has been implicated in the bioelectric response of bone marrow-derived macrophages (BMDMs). However, given the functional heterogeneity of macrophage populations, the specific response of tissue macrophages is less well characterized. In this study, we examined the regulatory effects of direct current electric field (dcEF) stimulation on NPFFR2 in primary thioglycolate-elicited peritoneal macrophages (TEPMs) by integrating cellular assays, transcriptomics, and molecular dynamics (MD) simulations. Our data indicate that dcEF intensities (25-200 mV/mm) elicited morphological polarization in TEPMs while maintaining metabolic viability. In contrast to the receptor downregulation typically observed in recruited BMDMs, dcEF exposure-particularly at 25 and 150 mV/mm-was associated with elevated NPFFR2 protein levels in wild-type TEPMs. Molecular dynamics simulations suggested that high-intensity electric fields might physically destabilize the NPFFR2 core domain, facilitating conformational unfolding. However, cellular assays concurrently revealed a net accumulation of the protein. Transcriptomic and biochemical analyses suggest that this accumulation may be attributed to a compensatory biosynthetic response, which appears to offset the heightened degradation pressure associated with structural instability. Together, these observations point to a distinct, cell-type-specific regulation of NPFFR2 by dcEF. We propose a model wherein protein accumulation in macrophages is maintained through the activation of bioenergetic and translational pathways, thereby counterbalancing field-induced physical vulnerability. - Source: PubMed
Publication date: 2026/07/18
Zhao MengyaFang YanweiChen YunfeiZuo ZiyiJohansson Nellie AliciaXu XinyueSun Yulong - This issue of the Biomedical Journal explores emerging perspectives across neuropsychiatry, metabolism, aging, regenerative medicine, artificial intelligence, and chronic inflammatory disease. Featured contributions examine epigenetic and neuroendocrine mechanisms in depression, including the antidepressant-like effects of magnolol in chronic stress-induced models and the potential relevance of short-chain fatty acids as biomarkers and therapeutic targets in major depressive disorder. Additional reviews address evolutionary and metabolic dimensions of liver disease, artificial intelligence-assisted imaging approaches in lymphedema, immunological senotherapeutic strategies, developmental origins of cardiovascular-kidney-metabolic syndrome, and the risks associated with short-term corticosteroid exposure. Original investigations further examine dopaminergic signaling during acute deprivation, molecular mechanisms of axonal regeneration, lipid peroxidation in pulmonary fibrosis, hypothalamic NPFFR2 signaling in metabolic dysfunction, neurobehavioral consequences of occlusal disharmony, and fall risk following cataract surgery with blue-light-filtering intraocular lenses. A correspondence exchange additionally discusses the diagnostic scope and limitations of elastase pretreatment in ALK fluorescence in situ hybridization analysis for non-small cell lung cancer. - Source: PubMed
Publication date: 2026/05/28
Kattner Aila Akosua - Neuropeptide FF receptor 2 (NPFFR2) plays a role in bioelectric field regulation in bone marrow-derived macrophages (BMDMs), but the influence of electric fields on NPFFR2 protein behavior remains unclear. This study investigates the effects of direct current electric field (dcEF) stimulation on NPFFR2 through cellular experiments and molecular dynamics (MD) simulations. The findings revealed that after applying physiologically relevant dcEF intensities (50 and 200 mV/mm) to wild-type and Npffr2-knockout BMDMs, cell viability was not significantly affected, but notable morphological changes occurred in both cell types. The dcEF stimulation suppressed NPFFR2 protein expression and induced cytoskeletal rearrangement in wild-type BMDMs. Furthermore, transcriptomic analysis revealed extensive gene expression changes, while MD simulations demonstrated that NPFFR2 conformation is sensitive to electric field strength in an intensity-dependent manner. Overall, these findings provide new insights into the interplay between a physical stimulus and a key immune receptor, suggesting that dcEF may regulate macrophage function by altering NPFFR2 protein levels and conformational stability. - Source: PubMed
Publication date: 2025/12/03
Zuo ZhuoWang YaxingZhao MengyaFang YanweiChen YunfeiZuo ZiyiSun Yulong