AKR1C4 Antibody
- Known as:
- AKR1C4 Antibody
- Catalog number:
- csb-pa001545esr2hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- 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
- Breast cancer remains the most prevalent cancer among women, driving the continuous search for novel anticancer agents. In this study, a series of 10-alkoxy steroids containing a 1,4-dien-3-one moiety was synthesized via a one-step dearomatization of the A-ring of estradiol and an estrane derivative with a D-homo lactone moiety. All compounds exhibited favorable in silico ADMET properties, while five derivatives showed significant cytotoxic activity in vitro. The strongest effects against the estrogen-positive breast cancer cell line MCF-7 were observed for two 10β-methoxy, one 10β-butoxy, and two 10β-propargyloxy derivatives. The activity of the 10β-butoxy-17β-hydroxy and 10β-propargyloxy-17β-hydroxy steroids correlates with strong binding affinity toward estrogen receptor α and inhibition of AKR1C3 and AKR1C4 enzymatic activity. Additionally, the propargyloxy derivative showed substrate-like binding to human recombinant aromatase. Molecular docking results are in qualitative agreement with these findings, predicting binding modes similar to known ligands and possible hydrophobic interactions between the C-10 alkoxy groups and the active sites of target proteins, particularly the heme group of aromatase. These results highlight novel estrane derivatives as promising candidates for estrogen-positive breast cancer therapy through combined effects involving AKR1C3 inhibition and interaction with aromatase and estrogen receptor. - Source: PubMed
Kuzminac IvanaBekić SofijaStevanović MilicaScholda JuliaKopp FlorianPetri EdwardĆelić AnđelkaSakač Marija - Aberrant lipid metabolism is closely associated with tumorigenesis and progression; however, its specific roles and molecular mechanisms in lung adenocarcinoma (LUAD) remain to be fully elucidated. This study aims to develop a prognostic signature based on lipid metabolism-related genes and to investigate the functional role of the key gene in LUAD. - Source: PubMed
Publication date: 2026/04/28
Li XianyongTang QianqianWang XuankaiLiu NaXu Jianjun - 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 not only functions 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
Goryszewska-Szczurek EwelinaWaclawik Agnieszka - BACKGROUND: Synthetic rescue (SR) interactions, where a disease-promoting alteration in one gene is compensated by a secondary alteration in another gene, remain largely unexplored in Alzheimer’s disease (AD). Here, we performed a genome-wide investigation of SR gene pairs that mitigate the genetic risk of AD. METHODS: Using whole exome sequencing (WES) data from the Alzheimer’s Disease Sequencing Project (ADSP) participants (n = 9,895), we first identified AD risk genes by two complementary methods: Single-variant analysis and Gene-wise Variant Burden (GVB) analysis. We then performed a genome-wide log odds ratio comparison to identify candidate SR gene pairs and further prioritized them via Cox proportional hazards regression. Validation and single-cell analyses were performed in the Religious Orders Study and Rush Memory and Aging Project (ROSMAP) cohort. RESULTS: Among the 37 candidate SR gene pairs, 27 pairs showing significant protective effects (HR < 1, FDR < 0.05) in Cox regression were prioritized. Notably, NR4A1, SULT2A1, AKR1C4, OR52H1, ARMC7, RBAK-RBAKDN, DMC1 for APOE, and LPP, ZNF510 for TREM2 reduced the hazard of AD onset by more than half. The prioritized SR pairs were validated in ROSMAP cohort using a synthetic rescue score (SRS) that quantifies the cumulative protective effect of rescuer genes against risk gene burden. We observed that SRS was significantly associated with delayed AD onset. In addition, SRS was significantly associated with better cognitive outcomes but not with neuropathological burden, suggesting that SR pairs may confer cognitive resilience. Functional enrichment and single cell analyses highlighted lipid and sterol metabolism in oligodendrocytes and astrocytes as a plausible biological mechanism of SR interactions in AD. CONCLUSIONS: Our study extends understanding of SR interactions in AD, implicating glial lipid and sterol metabolism as a key underlying mechanism and providing novel insights for therapeutic strategies beyond targeting AD risk loci. - Source: PubMed
Publication date: 2026/04/11
Yoo Jun KiKim Ju Han