Esrra antibody - C-terminal region (ARP32259_P050)
- Known as:
- Esrra (anti-) - C-terminal region (ARP32259_P050)
- Catalog number:
- arp32259_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Esrra antibody - C-terminal region (ARP32259_P050)
Related genes to: Esrra antibody - C-terminal region (ARP32259_P050)
- Gene:
- ESRRA NIH gene
- Name:
- estrogen related receptor alpha
- Previous symbol:
- ESRL1
- Synonyms:
- ERR1, ERRalpha, NR3B1, ERRa
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-25
- Date modifiied:
- 2016-10-05
Related products to: Esrra antibody - C-terminal region (ARP32259_P050)
Related articles to: Esrra antibody - C-terminal region (ARP32259_P050)
- E3 ubiquitin ligases are critical regulators of cell signaling and proteostasis that play a critical role in many diseases, including cancer. We aimed to investigate how E3 ubiquitin-protein ligase Casitas B-lineage lymphoma proto-oncogene C (CBLC) affects the development of endometrial cancer. Single-cell sequencing and bulk transcriptome analysis revealed a significant upregulation of CBLC expression in endometrial cancer cells. Functionally, CBLC accelerated the proliferation, migration, and invasiveness of endometrial cancer cells but suppressed their apoptosis. Mechanistically, CBLC ubiquitinated tRNA (guanine-N(7)-)-methyltransferase (METTL1), making it more stable and resistant to proteasomal degradation. METTL1 upregulation enhanced the N7-methylguanosine (m7G) modification of the estrogen-related receptor alpha (ESRRA) mRNA, enhancing its stability. ESRRA, in turn, mediated the pro-tumorigenic properties of CBLC. In conclusion, our study revealed that CBLC promotes the progression of endometrial cancer by orchestrating post-transcriptional and post-translational signaling cascades that stabilize METTL1 via ubiquitination and facilitate ESRRA m7G modification. These processes represent promising therapeutic targets for endometrial cancer. - Source: PubMed
Publication date: 2026/05/30
Peng JingweiZhang LinlinWang RuWang XiangyuLiu Ming - Optimizing ovarian superstimulation to improve oocyte quantity and quality is crucial for ovum pick-up and in vitro embryo production (OPU-IVP) in cows. In this study, we aimed to evaluate whether a single intramuscular injection of combined vitamin A, D, and E (VADE) during ovarian superstimulation enhances outcomes and milk yield in early lactation Holstein donor cows. Postpartum cows (40-60 days in milk) were randomly assigned to control (n = 79, superstimulation only) or VADE (n = 82, superstimulation + VADE injection at protocol initiation) groups. OPU-IVP outcomes, milk yield, and oxidative stress markers in serum, follicular fluid (FF), granulosa cells (GC), and oocytes were assessed. VADE supplementation significantly increased follicle number at OPU (34.3 vs. 27.0). It enhanced the number (8.9 vs. 6.2) and proportion (56.8% vs. 48.0%) of high-quality cumulus-oocyte complexes, leading to more blastocysts per donor (3.9 vs. 2.3). However, we did not observe that VADE helped restore milk yield during and after the ovarian superstimulation-OPU procedure. Transcriptomic analysis of GC revealed that VADE treatment downregulated genes involved in oxidative stress response. VADE treatment significantly reduced malondialdehyde levels in the serum and FF on OPU day, increased serum glutathione peroxidase activity, and decreased reactive oxygen species levels in the FF and oocytes. In addition, VADE treatment significantly downregulated ESRRA mRNA expression in GC. In conclusion, VADE supplementation during ovarian superstimulation improves oocyte quality and OPU-IVP efficiency in early lactation cows by alleviating oxidative stress, which is a readily implementable strategy for enhancing genetic utilization in high-yielding dairy herds. - Source: PubMed
Publication date: 2026/05/24
Xiao JinbangTian ManyuanDing ZhengjieMu HaohaoShe HaitaoLi HeqiangWang BingkeChen HuiJia YonghongWang YongshengJin YapingLin Pengfei - Lactate has been recognized as a major fuel substrate and also a lactyl-group donor for histone lysine lactylation. Hepatocytes act as lactate-consuming cells owing the high oxidative capability especially during exercise, a primary nonpharmacological intervention for alleviating metabolic dysfunction-associated steatotic liver diseases including steatohepatitis (MASLD/MASH). However, little is known regarding how lactate links the metabolic-epigenetic axis in hepatocytes. Here we show that declined estrogen-related receptor α (ESRRA) expression occur in MASLD/MASH accompanied with elevated levels of lactate and histone lactylation, particularly H3K18la. Such dysregulation can be partially rescued by chronic exercise in aged mice or exacerbated by genetic ablation of hepatocyte ESRRA. Mechanistically, exercise-induced ESRRA/PPARGC1A facilitates lactate consumption through transcriptional regulation of lactate dehydrogenase B and glucose-6-phosphatase catalytic subunit 1, rewiring lactate from a lactyl donor to gluconeogenic precursor in hepatocytes. Hepatocyte-specific ESRRA overexpression counteracts MASLD/MASH progression in mice, rectifying aberrant H3K18la accumulation and its marked gene transcripts that are involved in liver pathology. Our findings reveal that ESRRA functions as an exercise executor linking metabolism with epigenetic modification, highlighting a gluconeogenic-epigenetic regulatory axis that could be fine-tuned to mitigate risk factors of MASLD/MASH such as aging, menopause, a sedentary lifestyle and malnutrition. - Source: PubMed
Publication date: 2026/05/08
Gao JunYang MengDuan RuiHuang TonglingLi PengdaGao LuLu ZhaochengWong Chi-WaiGeng Chang-AnGuan Min - Osteoarthritis is an aging-related systemic disease involving the crosstalk of multiple organs/tissues in metabolism and inflammation, yet little is known about the contribution of liver and marrow adipose tissue (MAT). Here we show that MAT-derived complement factor D (CFD) and component 3 (C3) derived from steatotic liver coordinately drive excessive alternative complement activation, resulting in cartilage damage in mice during aging and metabolic disorders. Mechanistically, estrogen-related receptor α (ESRRA) transcriptionally upregulates CFD responding to bone marrow adipocytes (BMAds) expansion. Inhibition of ESRRA/CFD signaling in BMAds blocks the chondrocyte senescence and catabolism triggered by C3 that is released from steatotic hepatocyte, interrupting C3-CFD-MAC cascade, thereby suppressing ERK1/2 phosphorylation and mitochondrial dysfunction. Adipocyte-specific ablation or pharmacological inhibition of ESRRA reduces CFD levels particularly in adipocyte-rich bone marrow, attenuating osteoarthritis progression in aged mice. Our findings highlight a key liver-MAT-cartilage axis bridged by C3-CFD-MAC pathway, raising the potential for adipocyte ESRRA-targeting therapies for aging-related metabolic osteoarthritis. - Source: PubMed
Publication date: 2026/04/29
Huang TonglingWang ZihuiGao LuGao JunLu ZhaochengLi PengdaChoy Chon HimYuan ZhuoleiZhong YantingGeng Chang-AnWang HuaiyuYeung Kelvin W KLi BinPan HaoboChen DiGuan Min - NRF2 modulates tumor immune microenvironment in several cancers. NRF2 is activated in about 50% of high-grade serous ovarian cancer (HGSOC), the most aggressive type of ovarian cancer. Through analyzing data from scRNA-seq (n = 7), bulk RNA-seq (n = 365), and tumor microarray (TMA) of human HGSOC (n = 240) samples, we demonstrated that NRF2 expression correlated with tumor immune microenvironment in HGSOC. Functional pathway enrichment analysis and transcription factors (TFs) prediction showed the functional relevance of NRF2 expression in shaping the immune phenotype of HGSOC. Pathways such as hedgehog and ROS signaling, and TFs including EGR1, ESRRA, SMAD proteins, and SP-family proteins, are implicated in the immune suppressive microenvironment of NRF2 tumors. Immune differentiation analysis showed patients with NRF2 tumors enriched with CD68 have lower survival (p = 0.038) than those with CD68 tumors, whereas NRF2 tumors enriched with immune-activated markers such as CD3E and CD80 exhibit a better prognosis. This study is the first that shows classification of HGSOC based on NRF2 levels, highlights new biomarkers, and suggests IHC-labeling and genomic evaluation of NRF2 and immune markers for better prognosis. - Source: PubMed
Publication date: 2026/04/28
Hamad Samera HKatz ChelseaToma HelenMurakami KosukeBendjilali NasrineZhu GordShojaei HadiFang LanlanLeung SamuelKoebel MartinKaraduman HuseyinAbinader OliverMitra RamkrishnaKrill LaurenChu ChristinaWarshal David PWang Yemin