ADIPOR1 Antibody (C-term) Blocking Peptide
- Known as:
- ADIPOR1 Antibody (C-terminus) Blocking Peptide
- Catalog number:
- BP8634b
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ADIPOR1 Antibody (C-term) Blocking Peptide
Related genes to: ADIPOR1 Antibody (C-term) Blocking Peptide
- 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: ADIPOR1 Antibody (C-term) Blocking Peptide
Related articles to: ADIPOR1 Antibody (C-term) Blocking Peptide
- Clozapine, an atypical antipsychotic, is effective for treatment-resistant schizophrenia but frequently causes metabolic adverse effects, including hepatic lipid accumu-lation, inflammation and insulin resistance. Adiponectin, an adipocyte-derived cytokine with anti-inflammatory and insulin-sensitizing properties, may counteract these effects; however, its ability to mitigate clozapine-induced hepatic alterations remains unclear. This study examined whether adiponectin overexpression reduces clozapine-induced lipid accumulation, inflammatory signaling, and whether it restores insulin-related Akt signaling in human HepG2 liver cells. Cells were treated with 25 μM clozapine for 24 or 48 h, and adiponectin was overexpressed by plasmid transfection. Lipid accumulation was quantified by BODIPY staining. AdipoR1 and AdipoR2 expression was analyzed by qPCR, and protein levels of FASN, phosphorylated NF-κB, and phosphorylated Akt were assessed by Western blotting. Clozapine increased lipid accumulation, upregulated FASN, and reduced AdipoR1 and AdipoR2 expression. Adiponectin overexpression significantly decreased lipid levels, which was associated with reduced NF-κB phosphorylation, suggesting attenuation of inflammatory signaling. However, adiponectin did not restore insulin-stimulated Akt phosphorylation. In summary, adiponectin selectively reduced clozapine-induced lipid accumulation and inflammatory signaling in HepG2 cells, whereas impaired insulin-stimulated Akt phosphorylation remained unchanged under the present experimental conditions. These findings indicate a selective protective role of adiponectin and suggest its potential as a modulator of clozapine-induced metabolic side effects. - Source: PubMed
Publication date: 2026/07/20
Tsai I-LunLin Shih-ChaoLin LinTsai Pei-ShanChen Shiow-Yi - Skeletal muscle atrophy is a frequent comorbidity of metabolic disorders and chronic diseases, and despite its high prevalence, no pharmacological therapy is available, representing a major unmet clinical need. Adiponectin and its receptors are key regulators of skeletal muscle metabolism, mitochondrial function and myogenesis, yet clinical translation has been hindered by the lack of receptor-selective agonists with favourable pharmacological and safety profiles. Here, we report the identification and characterization of CDRI-1709S, the first small-molecule AdipoR1-selective agonist and evaluate its myogenic and anti-atrophy efficacy. - Source: PubMed
Moin Md RameezPal ShyamalDas ShubhrajyotiAwasthi PallaviTalukdar AnushkaKumar AkhileshVarode Shruti SuhasNikolas NikhilKhatoon ShamimaMugale Madhav NilkanthGuha RajdeepSanyal SabyasachiGoel Atul - Adiponectin is a pleiotropic adipocytokine with anti-inflammatory, antioxidant, and insulin-sensitizing functions. Its regulatory role in glucose and lipid metabolism, endothelial homeostasis, and immune responses positions it as a key determinant of immunometabolic resilience. Dysregulated adiponectin signaling has been increasingly implicated in adverse COVID-19 outcomes, particularly among individuals with metabolic comorbidities. - Source: PubMed
Publication date: 2026/07/21
Alqarni Ali AbdullahAl-Kuraishy Hayder MAlqarni MohammedEliwa DuaaAl-Gareeb Ali IBahaa Mostafa MBatiha Gaber El-Saber - Endothelial cell ferroptosis drives atherosclerosis. Salvianolic acid A (SAA), a polyphenol from Salvia species, was tested for its ability to inhibit ferroptosis and attenuate atherosclerosis, and its molecular mechanism was investigated. Screening of 124 natural compounds identified SAA as the most potent inhibitor of RSL3-induced ferroptosis in human umbilical vein endothelial cells (HUVECs). Cellular/mitochondrial lipid peroxidation, Fe content, ROS, and mitochondrial function were assessed with or without SAA. AMPK signaling was probed using pharmacological inhibitors. The AdipoR1 axis was examined via siRNA knockdown. In vivo, ApoE mice on a Western diet were treated with SAA to evaluate atherosclerosis and ferroptotic damage. SAA was identified as the most potent inhibitor of (1S,3R)-RSL3-induced ferroptosis in HUVECs among the screened natural compounds. SAA inhibited the ferroptotic response by restoring GPX4-dependent antioxidant capacity and preventing lipid peroxidation at both the cellular and mitochondrial levels. It improved mitochondrial function by restoring homeostasis of the mitochondrial quality control system, inhibiting mitochondrial reactive oxygen species generation, reducing ferrous iron accumulation, limiting mitochondrial lipid peroxidation, and preserving mitochondrial ultrastructure. The protective effects of SAA against ferroptosis were abolished by AMPK inhibitors, which disrupted cellular lipid metabolism and mitochondrial function regulation. The deleterious effects of AMPK inhibition were reversed by co-treatment with the mitochondrial reactive oxygen species inhibitor MitoTempol. Knockdown of AdipoR1 and experiments with the AMPK agonist AICAR confirmed that salvianolic acid A restores mitochondrial homeostasis and inhibits ferroptosis specifically through activation of the AdipoR1-AMPK signaling pathway. In vivo, treatment with SAA significantly ameliorated Western diet-induced atherosclerosis and ferroptosis-like cell damage in ApoE mice. SAA has strong therapeutic potential against endothelial ferroptosis and atherosclerosis by restoring mitochondrial homeostasis through AdipoR1-AMPK pathway activation. These findings support further clinical investigation of SAA for treating atherosclerosis and other endothelium-related cardiovascular diseases. - Source: PubMed
Publication date: 2026/07/17
Zhu JiGuo JiananLiu JingChen ChengChen HangWang CuiYuan AiniLu DezhaoLe Yifei - AdipoRon, a small adiponectin receptor (AdipoR) agonist, has the advantages of a low molecular weight, high stability, and long half-life. Preliminary data indicate that it also has anti-cancer effects. However, the investigation of AdipoRon in the context of ovarian cancer is limited. Further research is required to explore the underlying mechanisms. Cell function assays were performed to determine the effects of AdipoRon on the proliferation, apoptosis, migration, and autophagy of ovarian cancer cells. RNA sequencing was conducted on ovarian cancer cells treated with or without AdipoRon to identify dysregulated signaling pathways and targets. The effects of AdipoRon on AdipoR1/2, AMPK, its downstream genes, and autophagy in ovarian cancer cells were examined in the presence or absence of autophagy or AMPK inhibitors. Immunocompetent mice were used to establish an ovarian cancer metastasis model to evaluate the anti-tumor effects of AdipoRon. AdipoRon inhibited the proliferation and migration, promoted cell apoptosis, and induced autophagy in ovarian cancer cells in vitro. High-throughput transcriptome sequencing revealed a close correlation between autophagy and anti-tumor effects of AdipoRon. Mechanistically, AdipoRon induced autophagy by acting on the AdipoR1/2-AMPK-mTOR pathway, thereby inhibiting the progression of ovarian cancer. Blockade of AdipoR via shRNA, inhibition of autophagy or AMPK effectively rescued cells from AdipoRon-induced cellular phenotypes. Moreover, AdipoRon inhibited the malignant progression of ovarian cancer without noticeable loss of weight or organ side effects in an intraperitoneal transplant mouse tumor model. AdipoRon inhibited the malignant progression of ovarian cancer by inducing autophagy through the AdipoR1/2-AMPK-mTOR signaling pathway, suggesting its potential therapeutic value. - Source: PubMed
Publication date: 2026/07/08
Du HengweiLiu XueyuanHu RuiqiWang XinjingCui BingjieChen WeiweiWang FeiDong HongliangWang YiLiu CuilanDu Jing