Goat Anti-GPR81 _ FKSG80, with HRP-conjugated secondary antibody
- Known as:
- Goat Antibody toGPR81 _ FKSG80, horseradish peroxidase-labelled secondary detector ab (anti-)
- Catalog number:
- 126-10102
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Goat Anti-GPR81 _ FKSG80 with HRP-conjugated secondary antibody
Related genes to: Goat Anti-GPR81 _ FKSG80, with HRP-conjugated secondary antibody
- Gene:
- HCAR1 NIH gene
- Name:
- hydroxycarboxylic acid receptor 1
- Previous symbol:
- GPR104, GPR81
- Synonyms:
- HCA1, FKSG80, TA-GPCR, LACR1
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-20
- Date modifiied:
- 2015-09-11
Related products to: Goat Anti-GPR81 _ FKSG80, with HRP-conjugated secondary antibody
Related articles to: Goat Anti-GPR81 _ FKSG80, with HRP-conjugated secondary antibody
- Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disorder characterized by persistent fatigue and post-exertional symptom exacerbation, frequently associated with immune and metabolic disturbances. To evaluate the therapeutic potential of a probiotic formula, HH-205M, we employed a composite mouse model combining forced swimming stress (FSS) and repeated lipopolysaccharide (LPS) administration. FSS-LPS exposure induced pronounced fatigue-like phenotypes, including reduced physical endurance capacity in treadmill and weight-loaded swimming tests, delayed recovery in post-swim grooming behavior, and increased thermal pain sensitivity. These behavioral impairments were accompanied by elevated serum creatine kinase (CK), lactate dehydrogenase (LDH), and lactate levels, indicating systemic metabolic stress. At the tissue level, FSS-LPS increased lipid peroxidation and upregulated pro-inflammatory cytokine expression while suppressing antioxidant gene expression in the gastrocnemius muscle. Furthermore, expression of lactate-related genes, (GPR81) and (MCT1), was reduced, suggesting disruption of lactate transport and sensing pathways under chronic stress and inflammatory conditions. HH-205M supplementation attenuated the elevations in circulating fatigue-related biomarkers, moderated oxidative and inflammatory responses, and restored and expression. These molecular changes were paralleled by improvements in endurance performance and nociceptive sensitivity. HH-205M administration was also associated with distinct shifts in gut microbial composition, including enrichment of and and reduced relative abundance of . Collectively, these findings indicate that the FSS-LPS composite model recapitulates inflammation-associated metabolic disturbances relevant to fatigue-like conditions and that HH-205M administration is associated with concurrent improvements in behavioral and molecular parameters in this model. - Source: PubMed
Publication date: 2026/04/10
Song Jae GwangBae Hyun JinLee Dong HwanSeo JoeunLee BomiShin Kum-JooChung Eui-ChunLee JeongwookKim Hyung WookOh Nam Su - Astrocytes and tanycytes play essential roles in hypothalamic metabolic sensing, yet how glial-glial communication translates metabolic cues into neuronal activity remains poorly understood. We previously demonstrated that tanycytes release lactate and that this metabolite modulates the activity of arcuate pro-opiomelanocortin (POMC) neurons. Here, we identify the lactate receptor, HCAR1, as a key mediator of tanycytes-astrocyte-neuron signaling in the arcuate nucleus. We show that HCAR1 is highly expressed in hypothalamic astrocytes and present in a subset of NPY neurons. In primary hypothalamic cultures, L-lactate, the endogenous agonist of HCAR1, elicited increases in astrocytic cytosolic Ca and stimulated glutamate release; both effects were abolished by HCAR1 silencing using siRNA. In parallel, L-lactate and 3Cl-HBA increased connexin hemichannel activity, and hemichannel inhibition reduced glutamate release. Consistent with these in vitro observations, focal intracellular glucose delivery to a single tanycyte in acute hypothalamic slices triggered rapid Ca elevations in neighboring astrocytes, revealing functional glial-glial communication in situ. Importantly, activation of astrocytic HCAR1 enhanced NMDA receptor-dependent slow inward currents and excitability in POMC neurons, an effect reproduced by pharmacological HCAR1 agonists and abolished by astrocytic HCAR1 silencing. Together, these findings uncover a glial metabolic relay in which tanycyte-derived lactate activates astrocytic HCAR1, promotes glutamate release, and enhances POMC neuron excitability, providing a mechanistic link between cerebrospinal fluid-borne glucose fluctuations and hypothalamic control of feeding. - Source: PubMed
Publication date: 2026/04/07
López SergioElizondo-Vega RobertoAzócar VinkaSepúlveda VaniaOpazo-Mellado ValentinaVásquez WalterSáez Juan CAraneda Ricardo CGarcía-Robles María de Los Ángeles - Arenobufagin (ARBU), a steroid compound extracted from the venom of Bufo gargarizans, exhibits multi-target pharmacological activities, yet its role in regulating ferroptosis in gastric cancer stem cells (GCSCs) remains unclear. This study systematically evaluated the antitumor effects and mechanisms of ARBU using in vitro sphere culture, organoid models, and xenografts. ARBU inhibited GCSC proliferation and sphere formation in a concentration-dependent manner, reduced EdU incorporation and SOX2 expression in organoids, and markedly suppressed tumor growth in vivo while downregulating SOX2 and Nanog, with favorable biosafety. Mechanistically, ARBU induced ferroptosis, evidenced by elevated MDA, ROS, and Fe, decreased GSH and SOD, mitochondrial damage, COX2 upregulation, and GPX4/SLC7A11 downregulation. RNA-seq and functional studies further revealed that HCAR1 critically regulates GCSC self-renewal and antioxidant defense, and ARBU promoted ferroptosis via HCAR1 suppression. Collectively, these results demonstrate that ARBU inhibits GCSC proliferation and stemness by inducing ferroptosis through downregulation of the HCAR1 pathway, highlighting its potential as a therapeutic candidate for gastric cancer. - Source: PubMed
Publication date: 2026/03/17
Wang HainanWang NingGu WeiWang ManmanCheng HuiHe ShimingWang MengLi Qinglin - Glioblastoma (GBM) is a highly lethal brain tumor with limited treatment efficacy due to therapy resistance and the blood-brain barrier (BBB). Here, we developed tLyP-1-modified polyethylene glycol (PEG)-coated hollow catalase-mimicking MnO₂-based nanocarriers (HM@si-SLC16A1/TMZ-tLyP-1, tLyP-NPs) for the targeted co-delivery of temozolomide (TMZ) and SLC16A1 siRNA (si-SLC16A1). These nanoparticles generate oxygen through H₂O₂ decomposition, alleviating tumor hypoxia and enhancing MRI imaging via Mn²⁺ release. In vitro, tLyP-NPs exhibited high siRNA loading efficiency, pH-responsive drug release, and effective SLC16A1 silencing, leading to reduced glioma cell viability and enhanced apoptosis under both normoxic and hypoxic conditions. tLyP-1 modification facilitated BBB penetration and glioma targeting, as evidenced by increased cellular uptake in a BMEC-C6 glioma co-culture model. In an orthotopic GBM rat model, the nanoparticles demonstrated superior tumor accumulation, prolonged T1-weighted MRI contrast, and enhanced therapeutic efficacy compared to non-modified formulations. Mechanistically, SLC16A1 silencing induced intracellular lactate accumulation, suppressed lactate-stimulated HCAR1/PI3K/AKT signaling, and promoted apoptosis in both in vitro and in vivo models. Histological analysis showed extensive tumor necrosis, increased apoptosis (Caspase-3, TUNEL), reduced proliferation (Ki67), and alleviated hypoxia (HIF-1α). Survival analysis revealed significantly prolonged survival without systemic toxicity. Collectively, tLyP-NPs represent a promising multifunctional nanoplatform that integrates BBB penetration, TME-responsive drug release, and synergistic chemo-gene therapy for GBM treatment. - Source: PubMed
Publication date: 2026/03/16
Zhao HaitingMeng LiDu PengChen YunGong MengqiZan BoChen JiaxinZeng MengtingLiao Yiwei - Astrocyte-derived lactate, through the astrocyte-neuron lactate shuttle, fuels neuronal energy demands and acts as a signalling molecule promoting synaptic plasticity and memory consolidation. Lactate regulates neuronal excitability and expression of genes related to synaptic plasticity and neuroprotection, but the molecular mechanisms remain unclear. Using patch-clamp recordings in cultured cortical neurons we found that lactate enhances NMDA receptor currents (I), increasing their amplitude and decay time constant. Not reproduced by HCAR1 agonists, this modulation depends on monocarboxylate transporters and lactate dehydrogenase, requiring lactate entry, metabolic conversion to pyruvate and NADH formation within neurons. Disruption of intracellular calcium dynamics or inhibition of Ca/calmodulin-dependent protein kinase II (CaMKII) diminishes lactate's effects on I. Two redox-sensitive cysteine-containing sequences in the intracellular C-terminal domain of GluN2B subunit play a crucial role in the potentiation of NMDAR by lactate. Experiments in HEK cells demonstrate that functional CaMKII and GluN2B-containing NMDARs are necessary for lactate's effects. Mutations in GluN2B, that disrupt either CaMKII binding or cysteine-mediated redox regulation, abolish lactate's modulatory action. Immunoprecipitation experiments in neurons show that lactate promotes CaMKII-GluN2B association, which is critical for increasing I amplitude. Proximity ligation assays between GluN2B and PSD-95 reveal that lactate induces GluN2B accumulation in dendritic spines, an effect a CaMKII inhibitor prevents. These findings elucidate a pathway whereby lactate enhances NMDAR function through metabolic conversion and redox-sensitive interactions requiring CaMKII, linking astrocyte energy metabolism to synaptic modulation. KEY POINTS: Astrocytes produce lactate, traditionally seen as an energy source, which also acts as a signalling molecule in the brain, influencing memory and synaptic plasticity by modulating NMDA receptor (NMDAR) function. Lactate enhances NMDAR responses specifically by increasing current amplitude through changes in cellular redox balance, which requires the entry of lactate into neurons and its conversion to pyruvate, producing NADH. Lactate-induced potentiation of NMDARs depends on calcium signalling involving Ca /calmodulin-dependent protein kinase II (CaMKII), which interacts directly with the GluN2B subunit of the receptor. Lactate strengthens the interaction between CaMKII and GluN2B through redox-sensitive cysteine residues in GluN2B, facilitating synaptic localization of this complex and enhancing synaptic responses. These findings reveal a molecular pathway by which lactate, produced by astrocytes, can significantly influence neuronal activity and synaptic function, linking brain metabolism with learning and memory processes. - Source: PubMed
Publication date: 2026/03/11
Fiumelli HubertHerrera-López GabrielLemtiri-Chlieh FouadMottier LorèneGirgis JohnBen-Adiba CarineJourdain PascalCarrano NicolòMahmood HananOoi AmandaArold Stefan TLuca Monica DiGardoni FabrizioMagistretti Pierre J