ACRP30 headless, human
- Known as:
- ACRP30 headless, H. sapiens
- Catalog number:
- bc-114
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- ACRP30 headless human
Related genes to: ACRP30 headless, human
- Gene:
- ADIPOQ NIH gene
- Name:
- adiponectin, C1Q and collagen domain containing
- Previous symbol:
- ACDC
- Synonyms:
- ACRP30, AdipoQ, apM1, GBP28, adiponectin
- Chromosome:
- 3q27.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-26
- Date modifiied:
- 2016-10-05
Related products to: ACRP30 headless, human
Related articles to: ACRP30 headless, human
- Extended periods of skeletal unloading cause rapid and severe bone loss, structural weakening, and increased fragility. Unlike postmenopausal osteoporosis, disuse bone atrophy is only partially responsive to pharmacological treatments, making it a critical and unresolved medical challenge in both space- and Earth-based medicine. Here, we investigate and assess the dose-response to P7C3 during the transition of bone-derived mesenchymal stem cells to osteoblasts and adipocytes, and its effect during human preosteoclast differentiation into mature osteoclasts in vitro. We further evaluate the in vivo protective properties of P7C3 against pathological bone atrophy induced by mechanical disuse. Data demonstrates that multifunctional P7C3 selectively promoted osteogenesis while inhibiting osteoclast maturation and activity. Proteomic analyses indicate osteogenic augmentation via ↑FSTL-1 and ↓IL-10Rβ, adipogenic inhibition via ↓ADIPOQ and ↑NAMPT, and osteoclastic inhibition via ↓OPN, ↑BMP-7 and ↑OPG. Enrichment analyses suggest the positive regulation of MAPK, JAK/STAT, and Wnt signaling pathways. Transcriptomic data reveal P7C3-induced cell-selective alterations in transcriptional programs within mitochondrial DNA, potentially promoting ATP generation through NADH activity, and regulating cellular energy metabolism. Hindlimb suspension (HLS) induced rapid pathologic bone loss in vivo, with an overarching drive towards adipogenesis (↑C4.A4, ↑FABP3, ↑ADIPOQ, and ↓Dcn) over osteogenesis (↑activin R2A, ↑LIFR and ↓STAT3) and augmented osteoclastic activity and cellular senescence, potentially via MAPK, JAK/STAT, and Wnt signaling. Despite HLS, P7C3 attenuated oxidative stress, RANKL, osteoclastic activity, bone marrow adiposity, cellular senescence, and pathological bone loss. P7C3 presents as an undiscovered and promising multi-target therapeutic strategy against disuse-induced bone atrophy for both space- and Earth-based applications. - Source: PubMed
Publication date: 2026/10/03
Wei FeiNgo ChristopherNeal Craig JSchwartzman Jonathan DPugazhendhi Abinaya SinduOmer MahmoudWalck Christine DSeal SudiptaCoathup Melanie J - Non-alcoholic fatty liver disease (NAFLD) is a metabolic disorder characterized by lipid accumulation in hepatocytes. Our previous study demonstrated that the herbal pair (HS) of Astragalus Radix (HQ) and Dioscoreae Rhizoma (SY) reduces blood lipids and improves hepatic lipid metabolism in high-fat diet-fed mice. - Source: PubMed
Publication date: 2026/09/28
Miao JunjieNiu WanlinHuang BoShi ZhongfengWu Lirong - Brown adipose tissue (BAT) and beige adipocytes regulate adaptive thermogenesis and systemic energy balance, whereas BAT dysfunction contributes to obesity and metabolic disease. Although ETS transcription factors participate in adipocyte biology, the role of ETS-2 in BAT remains unclear. - Source: PubMed
Publication date: 2026/09/26
Chen HongjinZhai XinrongZhang YoujunChen KunFu LeiHu DonghuaZheng ZhiyuanGuan ShaofengQu XinkaiYe Maoqing - Diabetic kidney disease (DKD) is a leading cause of chronic kidney disease, and tubulointerstitial fibrosis (TIF) represents its final pathological hallmark. Progestin and adipoQ receptor 3 (PAQR3) has been implicated in metabolism and inflammation, but its role in DKD remains largely unexplored. Here, we report that PAQR3 expression is markedly upregulated in the kidneys of STZ-induced diabetic mice and in high glucose-stimulated NRK-52E tubular epithelial cells, correlating with the onset of tubular epithelial-mesenchymal transition (EMT) and fibrosis. Functional studies demonstrated that PAQR3 overexpression via AAV delivery in db/db mice significantly exacerbated renal dysfunction, fibrotic lesions, and EMT, whereas PAQR3 knockdown in cultured tubular cells attenuated the EMT phenotype. Mechanistically, PAQR3 selectively increased NOX4 protein levels without affecting its mRNA expression, leading to enhanced ROS production and oxidative stress. Notably, PAQR3 suppressed STUB1-mediated NOX4 ubiquitination, thereby stabilizing NOX4 protein. Collectively, these findings suggest that PAQR3 modulates NOX4 protein stability by suppressing its ubiquitination and the PAQR3-STUB1-NOX4 axis may contribute to TIF progression in DKD. - Source: PubMed
Publication date: 2026/09/26
Sun XiaohongTan ShiyunWu JiabiWang LirongWang Shaogui - Adipose tissue inflammation in obesity promotes insulin resistance and metabolic disease. The Duffy Antigen Receptor for Chemokines (DARC), a non-signaling receptor expressed on erythrocytes and on other cell types, modulates inflammation by regulating chemokine levels. Gene variants that affect DARC expression on erythrocytes are common in people of African descent. Here, we disrupted DARC expression in hematopoietic cells and adipocytes to determine the impact on obesity. - Source: PubMed
Publication date: 2026/09/15
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