Ask about this productRelated genes to: NR0B2 antibody
- Gene:
- NR0B2 NIH gene
- Name:
- nuclear receptor subfamily 0 group B member 2
- Previous symbol:
- -
- Synonyms:
- SHP
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-19
- Date modifiied:
- 2016-10-05
Related products to: NR0B2 antibody
Related articles to: NR0B2 antibody
- Anthocyanins are plant polyphenols widely regarded as antioxidants, yet they can exert concentration-dependent effects and act as pro-oxidants in specific contexts. Although their protective role in stressed testicular cells is established, their impact on Leydig cell steroidogenesis under non-pathological conditions remains poorly understood. Here, we investigated how an anthocyanin-enriched fraction from (0-1.00 μg/mL) affects androgen synthesis in murine TM3 Leydig cells. Cell viability, intracellular ROS, antioxidant capacity, mitochondrial function, androstenedione production, steroidogenic gene expression, and the exometabolome by H-NMR were assessed. The fraction exhibited biphasic, dose-dependent effects. At 0.01 μg/mL, it induced a mitohormetic response, upregulating mitochondrial complexes III and V. Conversely, higher concentrations (0.10-1.00 μg/mL) reduced metabolic activity, increased intracellular ROS, and significantly suppressed androstenedione synthesis independently of . These concentrations also induced dose-dependent repression of , concomitant with upregulation of , encoding the transcriptional repressor Small Heterodimer Partner (SHP). Overall, the data support a redox-dependent mechanism whereby elevated ROS promotes expression, leading to suppression and impaired androstenedione production. These findings challenge the view of anthocyanins as uniformly beneficial for male fertility and identify as a sustainable source of bioactive anthocyanins capable of modulating redox-endocrine homeostasis in a dose-dependent manner under basal conditions. - Source: PubMed
Publication date: 2026/04/23
Patanè Giuseppe TMoreira Ruben JMartins Ana DOliveira Pedro FPutaggio StefanoBarreca DavideAlves Marco G - T-2 toxin is a highly toxic mycotoxin commonly present in food and the environment, with accumulating evidence supporting its hepatotoxic potential. However, the molecular events linking T-2 toxin exposure to liver fibrosis remain insufficiently characterized. - Source: PubMed
Publication date: 2026/05/20
Qiao LichunShi ShaotengWang LiangjiaShafiq Muhammad AftabTang JingLi MiaoqianWan PingZhou JingxuanDai XuleiHan JingGuo Yijie - Natural light is severely affected by human impact on Earth, yet little is known about the roles light receptors have outside vision and rhythmic processes, despite their tremendously wide abundance. Here we show that loss-of-function of the () in marine bristleworms significantly increases lifespan and adult size, similarly to wild-types reared in constant darkness. Quantitative transcriptomics revealed hormonal players crucial for invertebrate and vertebrate sexual development and reproduction affected in mutants. These include , ortholog of () and (), long considered vertebrate novelties. Depending on moon-phase, is up- or down-regulated in mutants. Matching the complex regulation, data consistent with loss of function partially recapitulate phenotypes. Molecularly, Nr0b1/2 affects steroidogenic and other endocrine pathways, nuclear receptor signaling, and transcription factor orthologs involved in sexual developmental, reproductive, and timing processes in other organisms. Thus, our study suggests profound and direct effects of light on adult animal life-time, likely at least in part via conserved endocrine pathways involved in sexual maturation and reproduction in annelids and vertebrates. - Source: PubMed
Publication date: 2026/03/19
Andreatta GabrieleScaramuzza FedericoĆorić AidaOrel LukasMat Audrey MTakekata HirokiPoehn BirgitMilivojev NadjaTessmar-Raible Kristin - Osteoarthritis (OA), characterised by cartilage destruction, is the most common degenerative joint disease. However, no effective disease-modifying OA therapy is currently available. Herein, we report orphan nuclear receptor small heterodimer partner (SHP, NR0B2) as a novel catabolic regulator of OA pathogenesis. NR0B2 expression was markedly downregulated in cartilage from patients with OA. Global or chondrocyte-specific Nr0b2 deletion in male mice exacerbated OA-related pain and structural changes following surgical destabilization of the medial meniscus, accompanied by increased matrix metalloproteinase (MMP)-3 and MMP-13 expression in chondrocytes. Conversely, adeno-associated virus-mediated Nr0b2 overexpression in knee joints of male mice protected against accelerated knee OA caused by Nr0b2 deficiency. Mechanistically, NR0B2 inhibited IKKβ kinase activity via IKK complex interaction, downregulating NF-κB signalling. Our results demonstrate that NR0B2 has a chondroprotective role in OA progression by regulating matrix-degrading enzymes in an IKKβ/NF-κB-dependent manner, and gene therapy targeting Nr0b2 may be a promising therapeutic strategy for OA. - Source: PubMed
Publication date: 2026/02/21
Kang Eun-JungNoh Jung-RanKim Jae-HoonPark Ji AhAhn Jeong-PinKim Min-ChanChoi Jung HyeonChoi Young-KeunLee In-BokChoi Dong-HeeSeo Yun JeongJung Yoon SeokKim Kyoung-ShimHwang Jung HwanKim Yong-BumLee Jong-SooKu Bon JeongJeong Jin-OkChoi Hueng-SikKim JinhyunKim Yong-HoonLee Chul-Ho - Hepatocellular carcinoma (HCC), the common liver cancer, exhibits higher incidence in males. Here, we report that mice lacking bile acid (BA) regulators, Farnesoid X Receptor (FXR also termed NR1H4) and Small Heterodimer Partner (SHP also termed NR0B2), recapitulate the sex difference in liver cancer risk. Since few therapeutic options are available, we focused on understanding the intrinsic protection afforded to female livers. Transcriptomic analysis in control and NR1H4 and NR0B2 double knockout livers identified female-specific changes in metabolism, including amino acids, lipids, and steroids. To assess translational relevance, we examined if transcriptomic signatures obtained from this murine HCC model correlate with survival outcomes for HCC patients. Gene signatures unique to the knockout females correspond with low-grade tumors and better survival. Ovariectomy blunts the metabolic changes and promotes liver tumorigenesis in females that, intriguingly, coincides with increased serum bile acid (BA) levels. Despite similar genetics, knockout male mice displayed higher serum BA concentrations, while female knockouts excreted more BAs. Decreasing enterohepatic BA recirculation using cholestyramine, an FDA-approved resin, dramatically reduced the liver cancer burden in male mice. Overall, we reveal that sex-specific BA metabolism leading to lower circulating BA concentration protects female livers from developing cancer. Thus, targeting BA excretion may be a promising therapeutic strategy against HCC. - Source: PubMed
Publication date: 2025/12/29
Patton Megan EKelekar SherwinTaylor Lauren JDean Angela EZuo QianyingThakare Rhishikesh NLee Sung HwanGentry Emily CPanitchpakdi MorganDorrestein PieterAlnouti YazenMadak-Erdogan ZeynepLee Ju-SeogFinegold Milton JAnakk Sayeepriyadarshini