ADIPOR2 ELISA kit
- Known as:
- ADIPOR2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADIPOR2-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADIPOR2 ELISA kit
Related genes to: ADIPOR2 ELISA kit
- Gene:
- ADIPOR2 NIH gene
- Name:
- adiponectin receptor 2
- Previous symbol:
- -
- Synonyms:
- PAQR2, ACDCR2
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-23
- Date modifiied:
- 2018-05-03
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- Long-COVID syndrome is a public health issue, affecting millions of individuals worldwide. However, the pathophysiological mechanisms underlying the syndrome's sequelae are still under investigation. Adiponectin has been implicated with acute SARS-CoV2 infection, while its role in Long-COVID remains obscure. The aim of this study is to investigate the potential association of adiponectin and SNPs of adiponectin pathway with Long-COVID. - Source: PubMed
Publication date: 2026/04/08
Mavroudis PanagiotisRagia GeorgiaPantazis NikosDermitzaki EiriniStamati AlexandraPallikarou MyriaVelentza LemoniaPaflioti EleniZarkotou OlympiaGerakari StylianiGiannitsioti EfthymiaGravanis AchilleasManolopoulos Vangelis G - Psoriasis is a recurrent immune-mediated systemic disease. Adiponectin (APN), a key regulator of metabolism, is also known for its anti-inflammatory properties in several inflammatory disorders. The study aims to investigate the anti-inflammatory properties of APN on human immortalized keratinocyte cells (HaCaT) and to evaluate its therapeutic potential in an imiquimod (IMQ)-induced psoriasis mouse model. - Source: PubMed
Zhang LinglingKe ChunxiShen YunShi FengJiao QingqingJi Jiang - This study investigated whether ovarian adipokines exhibit uniform or stage-specific expression patterns across different follicular stages under hyperandrogenic conditions using a letrozole-induced polycystic ovary syndrome (PCOS) mouse model. Adult female mice received oral letrozole treatment for 21 days to induce hyperandrogenism, and ovarian tissues were analyzed by immunohistochemistry and western blot to examine the localization and expression of adiponectin (ADPN), adipoR1, adipoR2, leptin (Ob), leptin receptor (ObR), apelin (APLN), apelin receptor (APJ), chemerin, CMKLR1, and visfatin. Intense immunostaining for Ob, ObR, APJ, APLN, adipoR2, and visfatin was observed in primary, secondary, and Graafian follicles, whereas ADPN, adipoR1, and CMKLR1 showed reduced reactivity. In follicular cysts, adipoR2, APLN, APJ, and Ob were markedly upregulated compared with the corpus luteum of control ovaries, whereas ADPN, adipoR1, chemerin, CMKLR1, and ObR were downregulated. These findings indicate that hyperandrogenism disrupts adipokine signaling in a follicle-dependent manner, with differential expression patterns contributing to altered follicular maturation and cyst formation. The enhanced activation of adiponectin, apelin, and leptin signaling observed in cystic follicles may indicate disrupted adipokine-mediated regulation of ovarian physiology in letrozole-induced PCOS. Given the established roles of these adipokines in folliculogenesis and steroidogenesis, their dysregulation may contribute to follicular arrest and impaired ovarian function. These alterations are likely reflective responses to an altered endocrine and metabolic environment rather than direct causal mechanisms. Nonetheless, they may participate in the pathophysiological processes underlying cyst formation in PCOS. - Source: PubMed
Publication date: 2026/03/19
Dutta AyushmitaGurusubramanian GuruswamiRoy Vikas Kumar - Based on the adiponectin receptor/5'-AMP-activated protein kinase catalytic subunit α-1/carnitine palmitoyltransferase 1b(AdipoR/AMPKα/Cpt1b) signaling axis, this study investigated the therapeutic mechanisms of Jianpi Huogu Formula(JPHGF) in alcohol-induced osteonecrosis of the femoral head(AONFH). A total of 56 Sprague-Dawley rats were randomly divided into a normal group, a model group, and a JPHGF group(5.0 g·kg~(-1)). Except for the normal group, rats in the other two groups were administered 46% ethanol by gavage to establish the AONFH model, and JPHGF intervention was initiated in the treatment group at week 4 after model induction. After 4 and 8 weeks of intervention, samples were collected. Mechanical and cold pain thresholds were assessed using Von Frey filaments and the acetone drop test, respectively. Hindlimb muscle strength was evaluated by the inclined plane test. Micro-computed tomography(micro-CT) was used to determine bone mineral density(BMD), bone volume fraction(BV/TV), trabecular thickness(Tb.Th), and other bone morphometric parameters. Hematoxylin-eosin(HE) staining was performed to observe histopathological changes. Transcriptomic sequencing was conducted to identify differentially expressed genes(DEGs) regulated by JPHGF in AONFH, followed by Gene Ontology(GO) functional and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses. Western blot was used to detect the protein expression of AdipoR1, AdipoR2, phosphorylated AMPKα, and Cpt1b in femoral head tissues. The results showed that after 8 weeks of modeling, rats in the model group exhibited significantly decreased mechanical pain thresholds and increased cold sensitivity(P<0.05, P<0.01), indicating hyperalgesia. The maximum inclined angle was markedly reduced(P<0.01), suggesting weakened hindlimb muscle strength. The femoral head surface appeared rough, with enlarged dark-red cartilage areas and sparse, disrupted trabeculae; the proportion of empty lacunae and the number of adipocytes were significantly increased(P<0.01), while BMD, BV/TV, Tb.Th, and trabecular number(Tb.N) were significantly decreased(P<0.01). After 4 weeks of JPHGF intervention, mechanical and cold hyperalgesia were significantly alleviated(P<0.05), hindlimb strength was restored(P<0.01), and surface morphology of the femoral head was improved. After 8 weeks, trabecular structure was further restored, with decreased empty lacunae and reduced adipocyte numbers, and BMD, BV/TV, Tb.Th, and Tb.N significantly increased(P<0.05, P<0.01); cystic degeneration and collapse were markedly alleviated. Transcriptomic analysis revealed that JPHGF significantly regulated 231 key DEGs, which were mainly enriched in adipocytokine signaling pathways and closely associated with AdipoR1, AdipoR2, p-AMPKα, and Cpt1b. Western blot analysis showed that AdipoR1, AdipoR2, p-AMPKα, and Cpt1b expression levels were significantly downregulated in the AONFH model group compared with the normal group(P<0.01), but were markedly upregulated following JPHGF treatment(P<0.05, P<0.01). In summary, this study demonstrates that JPHGF exerts therapeutic effects against AONFH by activating the AdipoR/AMPKα/Cpt1b signaling axis, thereby improving bone marrow lipid homeostasis and restoring femoral head microarchitecture, effectively relieving pain and functional impairment. These findings provide new experimental evidence and molecular targets for the prevention and treatment of AONFH in clinical practice. - Source: PubMed
Chen Pei-PingHuang Feng-YuZhang Xin-ZhuoDing Dai-YueSong Chang-YueLiu Chun-FangKong Xiang-YingChen Wei-HengSu Xiao-HuiLin Na - Sarcopenia is an age-related condition characterized by the progressive decline of skeletal muscle mass and function. Although adiponectin is known for its anti-inflammatory and insulin-sensitizing effects that support muscle regeneration, paradoxically, elevated levels in older adults are linked to decreased muscle mass, strength, and performance. This study aimed to investigate the relationship between adiponectin levels, age, body composition, and functional status in elderly individuals, as well as to perform in vitro analyses of adiponectin resistance. - Source: PubMed
Publication date: 2026/03/05
Surina SurinaScisciola LuciaBasilicata Manuela GiovannaPesapane AdaFontanella Rosaria AnnaBalzano NunziaPalazzo Alberta Maria MaddalenaZia AsadTortorella GiovanniUlfat ZeeshanArshad MaryamJoshi RashmiVietri Maria TeresaCapuano AnnalisaPaolisso GiuseppeBarbieri Michelangela