AKR1C4 Antibody
- Known as:
- AKR1C4 Antibody
- Catalog number:
- AF1048a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- AKR1C4 Antibody
Related genes to: AKR1C4 Antibody
- Gene:
- AKR1C4 NIH gene
- Name:
- aldo-keto reductase family 1 member C4
- Previous symbol:
- CHDR
- Synonyms:
- DD4, HAKRA, C11, 3-alpha-HSD, CDR, MGC22581
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-26
- Date modifiied:
- 2016-06-03
Related products to: AKR1C4 Antibody
Related articles to: AKR1C4 Antibody
- L. (Rosaceae), belongs to a genus well recognized in traditional medicine for treating gynecological disorders and hormonal imbalance; however, the specific bioactivity of itself remains poorly characterized. This study aimed to elucidate the phenolic composition and the biological potential of the methanolic (MeOH) extract of . LC-MS/MS analysis identified 39 phenolic compounds, with rutin, catechin, kaempferol-3--glucoside, and caffeic acid being the dominant constituents. The extract exhibited high total phenolic and flavonoid contents, consistent with strong antioxidant capacities. It demonstrated notable α-glucosidase and acetylcholinesterase inhibitory activities, indicating its potential relevance for metabolic and neurodegenerative disorders. The extract effectively reduced AAPH-induced ROS levels in MRC-5 fibroblasts, indicating cytoprotective and antioxidative effects. The cytotoxicity toward cervical cancer cells HeLa and ovarian cancer cells A2780 was moderate and concentration dependent. A yeast-based fluorescent screen revealed a strong and selective binding affinity toward estrogen receptor α (ERα) and selective inhibition of human recombinant AKR1C3 (59.5%), without affecting AKR1C4. Additionally, high COX-1/COX-2 inhibition (>70%) supported its anti-inflammatory potential. Collectively, these findings provide the first integrated evidence of 's phenolic richness and multifunctional bioactivity, scientifically supporting its potential in managing hormone-dependent and oxidative stress-related disorders. - Source: PubMed
Publication date: 2026/03/26
Krstić SanjaBekić SofijaŽivanović NemanjaPirković AndreaVuković JovanaBauer RudolfRašeta Milena - Early pregnancy is a highly coordinated process requiring precise embryo-maternal communication. Estradiol-17β (E2) is considered the primary conceptus-derived signal responsible for the maternal recognition of pregnancy in pigs. Successful pregnancy establishment requires two distinct peaks of E2 secretion by porcine conceptuses: during days 11-12 (the maternal recognition of pregnancy) and days 15-30 (implantation). Although the role of E2 in signaling to the maternal system is well established, its potential autocrine effects on conceptus development remain unclear. This study examined whether E2 regulates trophoblast function during the maternal recognition of pregnancy and implantation. We demonstrated that expression of estrogen receptors (ESR1, ESR2, GPER1) and selected pregnancy-related genes (FOXO3, GDF15, SERPINE1, ESRRB, ESRRG) changes during early pregnancy in the pig. E2 regulated the gene expression of its receptors (ESR1, ESR2, GPER1), genes involved in E2 synthesis (HSD17B1), prostaglandin synthesis (PTGS2, AKR1C4, PTGES), and key mediators of pregnancy establishment (IL1B2, SERPINE1, FOXO3, GDF15, ESRRB and ESRRG). Furthermore, E2, acting via nuclear estrogen receptors, enhanced trophoblast cell proliferation on days 12 and 15 of pregnancy, and increased adhesion as well as MAPK1/3 and PTK2 protein phosphorylation on day 15 of pregnancy. E2 stimulated cell proliferation via MAPK and PI3K/AKT/mTOR pathways, whereas E2-promoted adhesion was mediated via MAPK and PI3K/AKT signaling. Concluding, these findings indicate that E2 functions not only as a critical embryonic signal for the maternal recognition of pregnancy but also plays an autocrine role in conceptus development, regulating gene expression and trophoblast cell function during early gestation in pigs. - Source: PubMed
Publication date: 2026/04/11
Goryszewska-Szczurek EwelinaWaclawik Agnieszka - Aging alters the systemic steroid environment, including reductions in circulating androgens. In peripheral tissues, androgen exposure is regulated mainly by local steroid metabolism, which can activate or inactivate androgens independently of systemic concentrations. In the scalp, 5α-reductase-mediated generation of dihydrotestosterone (DHT) has been studied extensively in relation to conditions such as androgenetic alopecia. In contrast, age-related regulation of DHT-inactivating pathways, including the aldo-keto reductase family 1 member C (AKR1C) family, remains insufficiently defined. - Source: PubMed
Publication date: 2026/04/07
Ikuno YasuakiKande YukieArakawa AkikoYamaguchi AkihikoTakahashi ToshifumiFujimoto NorikiNaka-Kaneda Hayato - Hyperuricemia (HUA) is a chronic metabolic disease which has been previously observed to be associated with cortisol metabolism disorders (pseudohypoadrenalism). In this study, we aimed to investigate the efficacy as well as mechanism of Eurycoma longifolia Jack (TkA) on alleviating cortisol metabolism. Oral administration of TkA significantly decreased serum uric acid levels and urinary cortisol in HUA mice. TkA improved HPA axis function and upregulated the levels of adrenal Hsd3b2, Cyp21a1 and Cyp11b1. In the liver, TkA upregulated the expression of Srd5a1 and Akr1c4, promoting the conversion from cortisol to 5α-tetrahydrocortisol (P < 0.001). TNFα was found to be the principal driver of reduced SRD5A1. By activating NF-κB pathway, recruited DNA methyltransferase (DNMT) binding with the CpG islands increased methylation level of Srd5a1. Our findings highlight that eurycomanol significantly inhibited the activation of IKKβ/IκBα/NF-κB/DNMT pathway as well as up-regulated hepatic SRD5A1, thereby restoring the systemic cortisol metabolic homeostasis under HUA. - Source: PubMed
Publication date: 2026/02/09
Pan JujieBao RuixiaChen QianWu YuzhengChen BeibeiZhu ZichengXie JingZhang YiWang TaoWang Dan - Among the disorders of sex development (DSD) with karyotype 46,XY, there is a group of diseases caused by defects of androgen synthesis. The last stage of in the synthesis of androgens is the conversion of testosterone into a more active androgen dihydrotestosterone, which occurs under the influence of the enzyme 5α-reductase type II (SRD5A2). SRD5A2 deficiency is a rare disease with autosomal recessive inheritance. - Source: PubMed
Publication date: 2025/12/02
Kalinchenko N YMakretskaya N AKolodkina A AKareva M ATiulpakov A N