ACACA_HUMAN ACCA ELISA tesk kit
- Known as:
- ACACA_HUMAN ACCA Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16522
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- ACACA_HUMAN ACCA ELISA tesk kit
Related genes to: ACACA_HUMAN ACCA ELISA tesk kit
- Gene:
- GPR3 NIH gene
- Name:
- G protein-coupled receptor 3
- Previous symbol:
- -
- Synonyms:
- ACCA
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-22
- Date modifiied:
- 2016-10-05
Related products to: ACACA_HUMAN ACCA ELISA tesk kit
Related articles to: ACACA_HUMAN ACCA ELISA tesk kit
- GPR3 belongs to the protein superfamily of G protein-coupled receptors (GPCRs) and plays a central role in both benign and malignant physiological processes, such as energy expenditure in adipocytes and Alzheimer's disease pathology, respectively. Despite the therapeutic potential of both receptor agonists and inverse agonists, GPR3 so far has lacked drug-like ligands and innovative screening technologies, hindering effective drug discovery efforts targeting this receptor. To overcome the limitations of conventional ligand screening techniques based on cAMP accumulation or β-arrestin recruitment, we developed a conformational GPR3 biosensor to monitor receptor activity in living cells with high-throughput screening (HTS)-compatible sensitivity and robustness. Combined with virtual compound screening against homology models of GPR3 and classical medicinal chemistry, this biosensor enabled us to identify new ligands, one of which (compound ) modulates GPR3-dependent G activity with an average potency in the nanomolar range. Our study not only presents novel GPR3 ligands for future optimization efforts and paves the way for even further expansion of the GPR3 ligand repertoire, but our sensor approach also provides a blueprint for targeting other therapeutically attractive yet challenging orphan GPCRs. - Source: PubMed
Publication date: 2026/05/07
Schihada HannesShahraki AidaTurku-Metsänen AinoleenaRath MaximilianWirth LukasNemec KatarinaTselepli HrisowalantuHeitzer LauraVallaster BernadetteFadel MariamSchulte GunnarHilger DanielPockes SteffenLohse Martin JKolb Peter - Rodents represent one of the key functional groups in ecosystems, and their population outbreaks can disrupt ecological equilibrium and cause substantial economic losses in agricultural production. Therefore, rational control of rodent populations is essential for maintaining ecosystem stability and minimizing economic damage. The striped hamster displays marked seasonal reproductive patterns, leading to significant fluctuations in population size across seasons. Investigating how female striped hamsters regulate follicle development in response to photoperiodic cues offers a promising target for the strategic management of pest populations. - Source: PubMed
Publication date: 2026/04/16
Xue HuiliangZhang XuetingQi WenFan ChaoXu JinhuiChen LeiWu MingXu Laixiang - Neuroinflammation, driven largely by microglial activation, is a core pathological feature of Alzheimer's disease (AD). Pathological tau species represent one of the key drivers of inflammatory activation in AD; however, the upstream regulators governing microglial inflammatory responses remain incompletely understood. Orphan G protein-coupled receptors (GPCRs) are emerging neuroimmune modulators, yet their specific roles in tau-mediated neuroinflammation are not fully characterized. This study investigated selected orphan GPCRs as modulators of this response. - Source: PubMed
Publication date: 2026/03/21
Sobhani AsmaSadr Narjes Khatoun ShabaniShahpasand KooroshMirnajafi-Zadeh JavadBehmanesh Mehrdad - GPR3 is a constitutively active Gs-coupled receptor whose transcriptional regulation during neuronal differentiation has remained unclear. Here, we identify as an immediate-early gene-like transcript rapidly induced by nerve growth factor (NGF) and cAMP signaling in PC12 cells, exhibiting biphasic activation captured by native elongating transcript-cap analysis of gene expression (NET-CAGE) at a core promoter ∼200 bp upstream of the transcription start site (TSS). Five cAMP response elements (CREs) within the 1-kb regulatory region cooperatively mediated stimulus-responsive transcription, with -CREB enrichment selectively occurring at the proximal -34 CRE. Early induction enhanced delayed expression and promoted () transcription through an -dependent mechanism. In primary cortical neurons, deletion diminished the developmental upregulation of and and reduced SYN1-positive vesicle density. These findings indicate GPR3 as an activity-dependent cAMP amplifier that couples early CREB activation to transcriptional programs governing NR4A signaling and presynaptic maturation during neuronal differentiation. - Source: PubMed
Publication date: 2026/02/07
Tanaka ShigeruIkawa FumiakiShiraki HirokoHarada KanaHide IzumiSakai Norio - Peripheral sensitization is a key process in the development of painful inflammatory conditions, driven in part by immune-cell mediator release following tissue injury. The G protein-coupled receptor, GPR183, predominantly expressed on immune cells, regulates their migration, positioning, and mediator production. Yet its role in peripheral sensitization and the specific immune cells involved remains insufficiently understood. In rats, intraplantar injection of 7α,25-dihydroxycholesterol (7α,25-OHC), the most potent endogenous GPR183 ligand, produced long-lasting nociception that was prevented by the selective GPR183 antagonist SAE-14. Because GPR183 activates ERK signaling, which influences pain pathways including nitric oxide synthase (NOS) activity and NO formation, we used NOS inhibitors and knockout animals to test the contribution of inducible and neuronal NOS isoforms to 7α,25-OHC-induced sensitization. We found that both isoforms influence this response, independent of cyclooxygenases. In a well-characterized rat incisional injury model, GPR183 protein expression increased in injured paw tissue, and SAE-14 reversed hypersensitivity. Meta-analysis of human post-surgical skin samples similarly showed elevated GPR183 expression and transcriptional changes favoring 7α,25-OHC production after injury. We identified macrophages and Langerhans cells (LCs) as the principal GPR183-expressing cell types in human skin. LC ablation studies revealed that 7α,25-OHC-evoked hypersensitivity does not depend on LCs, implicating GPR183 macrophages as predominant drivers of GPR3-induced hypersensitivity. Overall, our findings define the cellular and molecular pathways linking GPR183 to peripheral sensitization and highlight GPR183 antagonism as a promising strategy for pain management. - Source: PubMed
Publication date: 2026/01/16
Oberkrom KyleBraden KathrynLi EvelynShah Samay RMaric DraganMannes Andrew JPacifico PaolaJayaraj Nirupa DArnatt Christopher KMenichella DanielaSapio Matthew RSalvemini Daniela