Canine Adiponectin Receptor 1 ELISA , ADIPOR1
- Known as:
- Canine Adiponectin Receptor 1 Enzyme-linked immunosorbent assay test , ADIPOR1
- Catalog number:
- E08A0524
- Category:
- -
- Supplier:
- Blue Gene Biotech
- Gene target:
- Canine Adiponectin Receptor 1 ELISA ADIPOR1
Related genes to: Canine Adiponectin Receptor 1 ELISA , ADIPOR1
- Gene:
- ADIPOR1 NIH gene
- Name:
- adiponectin receptor 1
- Previous symbol:
- -
- Synonyms:
- PAQR1, ACDCR1
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-23
- Date modifiied:
- 2018-05-03
Related products to: Canine Adiponectin Receptor 1 ELISA , ADIPOR1
Related articles to: Canine Adiponectin Receptor 1 ELISA , ADIPOR1
- Adiponectin, a key regulator of peripheral lipid metabolism, exhibits a positive correlation between its reduced peripheral and central levels and cognitive function in Alzheimer's disease (AD). Previous studies suggest that adiponectin primarily crosses the blood-brain barrier to exert its neuroprotective and anti-inflammatory effects within the brain. However, the detailed mechanisms through which adiponectin improves cognitive function in AD remain unclear. This study found that APP/PS1 mice exhibited cognitive impairment accompanied by decreased peripheral adiponectin levels and reduced adiponectin receptor 1 (AdipoR1) expression in the hippocampus (with no change in AdipoR2 expression). Knockdown of AdipoR1 in the hippocampus induced cognitive impairment and neuroinflammation in C57BL/6 J mice. Overexpression of AdipoR1 improved cognitive function, suppressed microglial activation and expression of inflammatory factors, promoted β-amyloid (Aβ) clearance, and inhibited excessive synaptic phagocytosis by microglia in AD model mice. In vitro and in vivo experiments revealed that AdipoR1 may regulate the activation and function of hippocampal microglia in AD by modulating their autophagy to reduce abnormal lipid droplet (LD) accumulation. This study demonstrates that AdipoR1 is a highly promising therapeutic target for restoring lipid homeostasis in AD microglia, coordinating the regulation of their phagocytic function, and delaying disease progression. - Source: PubMed
Publication date: 2026/09/23
Li JingJiang LinChao FengleiZhang LeiHu ChunnianZhou YuningWang ShunPan QingLuo YanminTang JingLiang XinLi YueZhu PeilinDeng YuhuiLiu ShanQi YingqiangXiao QianTang YongZhou Chunni - Acquired aplastic anemia (AA) is an immune-mediated bone marrow failure syndrome characterized by destruction of hematopoietic stem and progenitor cells (HSPCs). Although HLA class II alleles are consistently associated with disease susceptibility, the candidate self-peptides presented by these molecules remain largely unknown. - Source: PubMed
Publication date: 2026/09/08
Correa Lara MaximilianoGarcía Chavez JaimeMartinez Hernandez Erika - To explore the role and mechanism of G-protein coupled receptor kinase 2 (GRK2)-mediated phosphorylation of adiponectin receptor 1 (AdipoR1) in diabetic cardiomyopathy (DCM), and to verify the therapeutic effect of site-directed mutagenesis targeting serine at position 205 (Ser205) of AdipoR1. Twenty 4-week-old C57BL/6J mice were randomly assigned to the normal control (NC) group and the DCM model group using a random-number table, with 10 mice per group. The DCM model was established in the DCM group by high-fat diet (HFD) feeding combined with intraperitoneal injection of streptozotocin (STZ). After 21-week intervention, 6 mice from each group were selected using a random-number table for measurements of serum biochemical parameters, adiponectin (APN) levels and cardiac diastolic function. Following euthanasia, myocardial tissues were harvested for Masson's trichrome staining to evaluate the degree of myocardial fibrosis. Co-immunoprecipitation and Western blot (WB) assays were performed to determine GRK2 expression, phosphorylated serine (p-Ser) levels, and the binding capacity between AdipoR1 and adaptor protein, phosphotyrosine-binding domain and leucine zipper motif 1 (APPL1). The remaining 4 mice per group were used for isolation of primary adult cardiomyocytes, which were treated with exogenous APN or phosphate-buffered saline (PBS). Phosphorylation status of the downstream adenosine monophosphate-activated protein kinase (AMPK)/protein kinase B (Akt) signaling pathway was subsequently detected. Twenty-eight 3-day-old AdipoR1-knockout neonatal mice were included in further experiments. Four of these AdipoR1-knockout neonatal mice were randomly selected by a random-number table to isolate primary cardiomyocytes. Plasmid co-transfection was conducted to assess AdipoR1-APPL1 interaction and downstream AMPK/Akt phosphorylation upon GRK2 overexpression. Four experimental subgroups were set: Adenovirus-empty(Ad-empty)+3×Flag-AdipoR1, Ad-empty+3×Flag-AdipoR1, adenovirus-mediated GRK2(Ad-GRK2)+3×Flag-AdipoR1, and Ad-GRK2+3×Flag-AdipoR1. This experiment aimed to identify whether Ser205 phosphorylation serves as the key molecular event whereby GRK2 blocks APN signaling. From the remaining 24 AdipoR1-knockout neonatal mice, 12 were randomly allocated into two groups (6 mice per group) using a random-number table. On postnatal day 3, mice received an injection of either adeno-associated virus serotype 9 (AAV9)-AdipoR1 or AAV9-AdipoR1. Ten weeks later, primary adult cardiomyocytes were isolated and divided into 4 subgroups: AAV9-AdipoR1+Ad-empty, AAV9-AdipoR1+Ad-GRK2, AAV9-AdipoR1+Ad-empty, and AAV9-AdipoR1+Ad-GRK2. GRK2 was overexpressed in vitro, and immunofluorescence co-localization was applied to quantify the co-localization of AdipoR1 and APPL1. The leftover 12 AdipoR1-knockout neonatal mice were randomized into two groups (6 mice per group) with a random-number table, and injected with the aforementioned viruses on postnatal day 3. Four weeks after virus injection, DCM was induced by HFD plus STZ administration, yielding two in-vivo groups: AAV9-AdipoR1+DCM (wild-type group) and AAV9-AdipoR1+DCM (point-mutation group). APN was continuously delivered via osmotic minipumps. Eight weeks after APN intervention, cardiac function and myocardial fibrosis were evaluated. In C57BL/6J mice, the DCM group exhibited significantly higher levels of blood glucose, triglycerides, low-density lipoprotein-cholesteral and adiponectin (APN) compared with the NC group (all <0.001). Statistically significant differences were observed between the two groups in the E/A ratio, radial strain rate, reverse radial strain rate (rRSR), longitudinal strain rate (LSR), and reverse longitudinal strain rate (rLSR) (all <0.05). The fraction of myocardial fibrotic area was larger in the DCM group than in the NC group (9.20±1.66 vs 1.24±0.51, <0.001). Myocardial protein levels of GRK2 (4.81±0.46 vs 1.03±0.09, <0.001) and p-Ser (1.75±0.21 vs 0.98±0.05, <0.001) were elevated in the DCM group relative to the NC group. The binding ratio of APPL1 to AdipoR1 in myocardial tissue was decreased in the DCM group versus the NC group (0.398±0.085 vs 0.978±0.088, <0.001). APN-stimulated AMPK/Akt phosphorylation was blunted in primary adult cardiomyocytes isolated from DCM-model C57BL/6J mice. In-vitro experiments using AdipoR1-knockout neonatal mouse cardiomyocytes demonstrated that following AdipoR1 Ser205 site mutation, the ratios of p-AMPK/AMPK (4.025±0.767 vs 1.003±0.087, <0.001) and p-Akt/Akt (4.125±0.544 vs 0.990±0.034, <0.001) were markedly increased in the 3×Flag-AdipoR1+APN group compared with the 3×Flag-AdipoR1+PBS group. In primary adult cardiomyocytes derived from AdipoR1-knockout mice, the AAV9-AdipoR1+Ad-GRK2 group restored the AdipoR1-APPL1 interaction in the presence of GRK2 when compared with the AAV9-AdipoR1+Ad-GRK2 group (=0.014). In the in-vivo DCM model established in AdipoR1-knockout mice, the AAV9-AdipoR1+DCM group displayed higher E/A ratio, rRSR, LSR and rLSR values, together with a lower myocardial fibrotic area fraction (all <0.05), relative to the AAV9-AdipoR1+DCM group. GRK2-mediated phosphorylation of AdipoR1 at serine 205 triggers APN-AdipoR1 metabolic dysfunction, which represents a critical contributor to aggravated cardiac dysfunction in DCM. This mechanism is associated with the decoupling of AdipoR1 from APPL1. Targeted inhibition of AdipoR1 phosphorylation via site-directed mutagenesis restores APN-AdipoR1 signaling and ameliorates cardiac dysfunction in DCM. - Source: PubMed
Yang Z JHu S CZhu DZhang Z YKang Y FTian Y MZhang LYe QFang L M - Atrial fibrillation (AF) is associated with obesity and epicardial adipose tissue (EAT) dysfunction. Although glucagon-like peptide-1 receptor agonists (GLP-1 RAs), such as liraglutide, exert cardiovascular benefits, the underlying mechanisms, particularly those related to EAT and adipokine signaling remain unclear. - Source: PubMed
Publication date: 2026/09/08
Li XinningLiu YanmengWang FanZhang FeifeiZhang LinaDang YiQi Xiaoyong
- Source: PubMed