HOXA10 antibody - N-terminal region (P100932_T100)
- Known as:
- HOXA10 (anti-) - N-terminal region (P100932_T100)
- Catalog number:
- p100932_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HOXA10 antibody - N-terminal region (P100932_T100)
Related genes to: HOXA10 antibody - N-terminal region (P100932_T100)
- Gene:
- HOXA10 NIH gene
- Name:
- homeobox A10
- Previous symbol:
- HOX1H, HOX1
- Synonyms:
- -
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2015-08-25
Related products to: HOXA10 antibody - N-terminal region (P100932_T100)
Related articles to: HOXA10 antibody - N-terminal region (P100932_T100)
- Benzo(a)pyrene (BaP), a ubiquitous environmental pollutant, exerts reproductive toxicity by disrupting endometrial decidualization, yet the underlying mechanisms remain unclear. This study aimed to dissect the molecular cascade linking BaP-induced oxidative stress to abnormal endometrial stromal cell (ESC) proliferation and decidualization injury. Pregnant mice were gavaged with 0.2 mg kg·day BaP from gestational Day 1 to 7, and primary ESCs were treated with BaP, HO, NAC and different inhibitor/agonist in vitro. BaP exposure reduced embryo implantation sites, induced asymmetric embryo distribution in bilateral uterine horns, and down-regulated decidualization markers (FOXO1, BMP2, HOXA10) in vivo and in vitro. Concurrently, BaP up-regulated proliferation markers (PHH3, PCNA, Ki67) and EdU incorporation in ESCs. Mechanistically, BaP induced uterine oxidative stress by down-regulating antioxidant enzymes (GPx4, CAT, SOD2) and accumulating intracellular ROS. HO recapitulated BaP-induced phenotypes, while NAC reversed these effects. BaP-induced oxidative stress activated the PKCα/KEAP1 pathway, promoting Nrf2 phosphorylation and nuclear translocation. Inhibition of PKCα by PKC-IN-6 alleviated BaP-induced Nrf2 activation. Activated Nrf2 up-regulated transketolase (TKT) and glucose-6-phosphate dehydrogenase (G6PD), key enzymes of the pentose phosphate pathway (PPP), to drive abnormal ESC proliferation. ML385 inhibited Nrf2 to rescued BaP-induced ESC hyperproliferation and decidualization injury, while SFN activated Nrf2 mimicked BaP's toxic effects. Collectively, BaP induces oxidative stress in early pregnancy uteri, sequentially activating the PKCα/KEAP1/Nrf2 pathway and G6PD and TKT, leading to ESC proliferation-differentiation imbalance and decidualization impairment. This study uncovers a novel oxidative stress-mediated mechanism of BaP reproductive toxicity, identifying Nrf2 and PPP enzymes as potential therapeutic targets for pollutant-related pregnancy disorders. - Source: PubMed
Publication date: 2026/04/10
Jiao FurongMa MengweiPeng LinglinLuo XinyanTong MingjieYi TingLong FengGao RufeiHan FeiHe JunlinXu HantingChen Xuemei - Copper and levonorgestrel-releasing intrauterine devices (IUDs) primarily prevent pregnancy through pre-fertilization mechanisms; however, their potential effects on endometrial receptivity remain incompletely understood. This study aimed to compare the regulation of selected adhesive and anti-adhesive endometrial receptivity markers in women using copper and levonorgestrel-releasing IUDs. - Source: PubMed
Publication date: 2026/03/30
Karakelleoğlu Gökçenur - Qi Gong Wan (QGW) is a herbal formula which is used for treating infertility associated with polycystic ovary syndrome (PCOS). However, the mechanism of action remains unclear. This study aimed to investigate whether QGW enhances endometrial receptivity in a PCOS with insulin resistance (PCOS-IR) rat model and to explore the underlying molecular mechanisms and primary active constituents. - Source: PubMed
Publication date: 2026/03/03
Ding ChunLi QinhuaDeng YiwenLiu YuhanLiu LeiCao ChunYuLi SiweiZheng TingtingXie LiangqunZhao JingYe HongLi Junkui - Whether endometriosis is a progressive disease remains debated. Central to this debate is understanding the natural history of endometriotic lesions, which are essentially wounds undergoing repeated tissue injury and repair. Viewing the disease through this lens, we reassess the literature on the progression, or absence thereof, of endometriosis and offer our perspective on this debate by delineating the aggravating and mitigating factors that influence lesional progression. We propose that the degree of lesional fibrosis, measurable via elastography as lesional stiffness, represents a promising marker for progression, as it correlates with aberrant histology, molecular alterations, symptom severity, clinical prognosis, and lesional mechanobiology. Lesional stiffness could aid in diagnosis, guide treatment choice, and predict outcomes, providing a valuable tool for managing endometriosis. - Source: PubMed
Publication date: 2026/03/20
Guo Sun-WeiCanis MichelVercellini Paolo P - - Source: PubMed
Publication date: 2026/03/19
Dong JingLiu XishiGuo Sun-Wei