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
- 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: 2026/09/25
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
Aboud GhaithBenson Tyler WHarb RaghebVeerapaneni PraneetZhang GuangweiAhmadieh SamahAgrawal RishabhGreenway CharlotteSellers HunterGoo BrandeeKim David SOgbi MouradCave StephenSharma MehekLiu LinglingHedrick Catherine CRobichaud SabrinaShi HongGuha AvirupHarris Ryan AWang XiaolingStepp DavidLei YunDu QuangshengKim Ha WonLu Xin-YunWeintraub Neal L - Polymorphisms in genes involved in obesity-related metabolic pathways are associated with metabolic syndrome (MetS). We hypothesized that variants in FTO, LEP, LEPR, ADRB3, ADIPOQ, TCF7L2, ENPP1, APOA5, PPARG, and CYP11B2 are associated with MetS and obesity-related traits. - Source: PubMed
Publication date: 2026/09/21
Stefani Tamiris Invencioni MoraesHirata Thiago Dominguez CrespoCerda Alvarode Oliveira RaquelDos Santos Marina AparecidaFajardo Cristina MorenoDorea Egídio LimaBernik Márcia Martins SilveiraHirata Mario HiroyukiHirata Rosario Dominguez Crespo - Aging disrupts the coupling between redox homeostasis and energy metabolism in brown adipose tissue (BAT), but the molecular nodes linking BAT redox-metabolic deterioration to systemic metabolic dysfunction remain unclear. Using aging mouse BAT time-course transcriptomics, we prioritized Acss1, encoding mitochondrial acetyl-CoA synthetase 1 (ACSS1), as a progressively age-decreased mitochondrial metabolic candidate. Acss1 expression correlated positively with BAT metabolic programs and negatively with oxidative stress and senescence-associated programs. Age-series single-nucleus transcriptomics further localized Acss1 mainly to adipocytes and classified BAT adipocyte nuclei into Acss1-high and Acss1-low transcriptional states. Acss1-high adipocytes retained thermogenic, oxidative phosphorylation and fatty acid oxidation programs, whereas Acss1-low adipocytes were enriched for stress- and senescence-related programs, with this divergence increasing with age. To test Acss1 function, we locally injected 18-month-old mouse BAT with an adeno-associated virus expressing Acss1 under the adipocyte-specific adiponectin (Adipoq) promoter. BAT-local Acss1 restoration attenuated redox imbalance, restored thermogenic programs and reduced senescence-associated injury. This local intervention also improved glucose and lipid metabolism, energy substrate utilization, motor performance and plasma antioxidant capacity, and was associated with improved histological and stress-related features in distal metabolic tissues. Matched BAT transcriptomic and plasma metabolomic profiling showed that Acss1 restoration shifted BAT redox-metabolic programs and was associated with spermidine-related circulating metabolic remodeling. In human BAT, ACSS1 expression correlated positively with oxidative phosphorylation and negatively with reactive oxygen species metabolic processes. These findings support brown adipocyte Acss1 as a regulator of redox-metabolic homeostasis in aged BAT, whose restoration is associated with improved local BAT state, improved systemic metabolic phenotypes and spermidine-related circulating metabolic remodeling. - Source: PubMed
Publication date: 2026/09/18
Luo YuchengZhang YuchenSong YuangLi XiangtianLiang JiancongXing HaonanLai YujinChen YinuoZeng MinxiZhou ChengChen HuishanWang WenqiLi YeLi BinLu FengDong Ziqing - Hypothermia is a life-threatening condition lacking specific pharmacological treatments. This study aimed to prioritize genetically supported molecular loci associated with hypothermia and to explore their pharmacological tractability using multi-omics data. - Source: PubMed
Publication date: 2026/09/15
Ran ShuShi XiaolongZhang JinbaoPeng HaoLi Yuehua