Ask about this productRelated genes to: GPR56 antibody
- Gene:
- ADGRG1 NIH gene
- Name:
- adhesion G protein-coupled receptor G1
- Previous symbol:
- GPR56
- Synonyms:
- TM7LN4, TM7XN1
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-12
- Date modifiied:
- 2015-03-03
Related products to: GPR56 antibody
Related articles to: GPR56 antibody
- Immune checkpoint (IC) pathways play a central role in modulating HIV-specific T cell responses and may influence the degree of viral control. Here, we performed a comparative transcriptomic analysis of CD4⁺ T cells from HIV-infected individuals classified as elite controllers (EC), viremic controllers (VC), and chronic progressors (CP), aiming to identify IC signatures associated with viral control. ECs exhibited distinct expression profiles, characterized by significant upregulation of and (), and downregulation of , , , , and relative to CPs. VC samples displayed intermediate expression levels. Principal component analysis (PCA) of IC genes revealed clear separation between ECs and CPs, driven largely by the differential expression of , , , and . ECs were also enriched in effector memory and Th2 CD4⁺ T cell subsets, which correlated positively with and , and inversely with and . Co-expression network analysis identified two distinct gene modules: one (M2) containing and , enriched for interferon signaling and NF-κB pathways, and another (M4) comprising , , and , enriched for TCR signaling and metabolic processes. Finally, comparison of ECs, ART-naïve, and ART-treated individuals showed that pre-ART subjects displayed significantly elevated expression, which decreased following ART initiation, resembling the EC profile. These findings reveal checkpoint-related molecular signatures and cell subset compositions that stratify HIV-infected individuals by disease control phenotype, and highlight potential targets for immunomodulatory therapies aimed at achieving functional cure. - Source: PubMed
Publication date: 2026/04/29
Spampinato SerenaScuderi GraziaDi Rosa MichelinoFagone PaoloNunnari Giuseppe - Adhesion G protein-coupled receptors (AGPCRs) regulate essential physiological processes through interactions between their ectodomains and adjacent cell surface proteins or extracellular matrix components (ECM). AGPCRs distinctively arrive at the plasma membrane as self-cleaved holoreceptors with noncovalently associated N-terminal (NTF) and C-terminal fragments (CTF). Canonical AGPCR signaling proceeds in three sequential steps; NTF adhesive domains bind to ligands, extracellular shear force mediates NTF and CTF dissociation, a tethered peptide agonist (TA) is exposed and binds to the CTF orthosteric site to stabilize the active state receptor. Depending on the cellular context, both autoproteolysis-deficient and perhaps, a few cleavage-capable AGPCRs may be activated without NTF dissociation or the action of the TA. To discriminate the functional consequences of these signaling modes in vivo, we created a cleavage-deficient, H381S knock-in mouse and investigated five distinct defective phenotypes of knockout mice. One prominent phenotype, brain malformation that parallels human bilateral frontoparietal polymicrogyria (BFPP) disease, is characterized by dysplasia of the cortex and cerebellum and neuron heterotopia. Brain histology analyses confirmed that H381S mice had comparable cerebellar structural irregularities as knockout mice, indicating that TA agonism is indispensable for proper cerebellar lobule formation and neuronal migration. TA-dependent signaling was also required for male mouse fertility, but not for adult cardiomyocyte homeostatic functions, platelet-dependent hemostasis, or axon myelination in the central nervous system. These findings indicate that GPR56 has multiple modes of activation and that these signaling outcomes are likely driven by NTF interactions with specific ligands including collagen and transglutaminase-2. - Source: PubMed
Publication date: 2026/04/22
Kwarcinski Frank EBernadyn Tyler FTeuber James PNascimento MarianeBergin IngridShen TingzhenGandhi RiyaLu XinyiBrody Matthew JHolinstat MichaelTall Gregory G - Cervical spondylosis and low back pain caused by intervertebral disc degeneration (IVDD) are among the leading causes of clinical disability. Although excessive reactive oxygen species (ROS) are established drivers of IVDD, the mechanisms linking ROS accumulation to disc cell dysfunction, cell death programs, and disruption of intervertebral disc tissue homeostasis remain insufficiently elucidated, limiting the development of effective redox-targeted therapies. Here, we revealed the "ROS-Mitochondrial dysfunction-Ferritinophagy" oxidative stress feedback loop serves as the central mechanism driving ROS-induced nucleus pulposus cell (NPC) ferroptosis to promote IVDD progression. Furthermore, we identified the membrane protein ADGRG1 as a biomarker of ROS-induced ferroptosis in injured NPCs and developed ADGRG1-tethered peptide (A1TP)-modified hypoxia preconditioned extracellular vesicles (HX-EVs) with targeted antioxidant therapeutic potential. The engineered HX-EVs selectively accumulated in injured NPCs and delivered high levels of taurine, which bound to LKB1 (Glu165, Arg301) and MO25 (Arg194, Leu197) residues to facilitate the assembly of the LKB1-STRAD-MO25 kinase complex. This interaction regulated the expression of NCOA4 and TFAM by activating the AMPK/NRF2 signaling pathway, which suppressed ferritinophagy, enhanced mitochondrial repair and regeneration, and protected NPCs from ROS-induced ferroptosis, ultimately facilitating the repair of degenerated intervertebral discs. In summary, the A1TP-HX-EV system developed in this study provides a promising theranostic application for IVDD and offers valuable insights into the mechanisms of targeted HX-EV delivery and intervertebral disc regeneration. - Source: PubMed
Publication date: 2026/02/18
Chen ShangJia ShuFan XutaoZhu LaiminQi BaoYan FenglianGao XuZhang LuGao ShengShao JunYang TaoLi ShudongChen GuowuXiong HuabaoLi ZongjinHao YankeMeng Chunyang - Brain-resident macrophages (BRMs), including microglia and border-associated macrophages (BAMs), are the core immune sentinels of the central nervous system (CNS). They originate from early embryonic yolk sac and fetal liver progenitors and maintain their population throughout life via self-renewal. During neurodevelopment, microglia maintain neural network homeostasis by phagocytosing apoptotic neural precursors and pruning synaptic connections. In adulthood, they rapidly respond to infection, injury, or protein aggregation, which can both promote repair and exacerbate neurotoxicity. BAMs, located in the meninges, perivascular spaces, and choroid plexus, play a key role in boundary homeostasis and peripheral immune signal surveillance. Recent studies reveal that BRMs exhibit dual roles in Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), multiple sclerosis (MS), as well as ischemic stroke, traumatic brain injury, and radiation-induced brain injury: they can protect neurons by clearing pathological proteins or cellular debris, but persistent inflammatory responses may drive neurodegeneration. In AD, microglia clear Aβ plaques via triggering receptor expressed on myeloid cells 2 (TREM2) and ADGRG1 signaling, while BAMs regulate synaptic damage and cerebrovascular function through CD36-ROS and SPP1 pathways. In PD and HD, BRMs contribute to -synuclein- and mutant huntingtin-related inflammatory responses. In MS, BRMs modulate the pro-/anti-inflammatory balance through antigen presentation and cytokine signaling. Based on these mechanisms, therapeutic strategies targeting BRM functions are emerging, including NLRP3 inflammasome inhibitors, TREM2 agonists, and interventions promoting microglial neuroprotective phenotypes. Future approaches aiming to precisely modulate BRM plasticity and their interactions with the peripheral immune system may transform these immune sentinels from "disease drivers" to "therapeutic allies," offering novel strategies for treating neurodegenerative diseases and brain injuries. - Source: PubMed
Publication date: 2026/02/09
Zhao PengLi Su-YiLiu QunPeng Xiao-ChunLiu LianYang Fu-YuanWang ChaoQian FengTang Feng-Ru - The adhesion G-protein coupled receptors (aGPCRs) are a family of 33 G-protein receptors consisting of ADGRA1-3, ADGRB1-3, ADGRC1-3, ADGRD1-2, ADGRE1-5, ADGRF1-5, ADGRG1-7, ADGRL1-4, and ADGRV1. Recent studies have unveiled the role of aGPCRs in numerous brain functions, including in neurodevelopment, synapse formation and maintenance, establishment of the blood-brain barrier, and myelination. Further, dysfunction of aGPCRs have been associated with disorders such as gliomas, depression, and epilepsy, among many others. Herein, we review generalized properties of aGPCRs, their brain-specific expression, associations with neurological and psychiatric diseases, and potential as future pharmacological targets. - Source: PubMed
Publication date: 2025/11/24
Lee Brandon HMeyer Christina MSpeca David JDíaz Elva