HOXA10 Antibody (Center)
- Known as:
- HOXA10 Antibody (Center)
- Catalog number:
- AP10276c
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- HOXA10 Antibody (Center)
Related genes to: HOXA10 Antibody (Center)
- 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 (Center)
Related articles to: HOXA10 Antibody (Center)
- Polycystic ovary syndrome (PCOS) is a highly prevalent and phenotypically diverse endocrine disorder in which insulin resistance (IR) serves as a central molecular driver of major metabolic and reproductive complications, including infertility, obesity, and increased long-term cardiovascular risk. This review examines the complex pathophysiology of PCOS, emphasizing how chronic systemic low-grade inflammation, gut microbiome dysbiosis, and oxidative stress interact to worsen hyperinsulinemia and hyperandrogenemia. It also highlights the clinical value of emerging diagnostic and prognostic biomarkers to improve risk stratification and patient management. Systemic biomarkers, such as pro-inflammatory cytokines, circulating endotoxemia arising from increased intestinal permeability, and epigenetic regulators including miR-146a, may provide prognostic insight into the trajectory of metabolic deterioration. In parallel, endometrial biomarkers, including the glucose transporter GLUT4, implantation-associated genes such as HOXA10, and inflammatory mediators like TNF-α, can support evaluation of impaired uterine receptivity, prediction of assisted reproductive technology (ART) outcomes, and stratification of miscarriage risk. By mapping key interactions within the gut-immune-metabolic axis and detailing localized endometrial dysfunction, this review proposes a framework for integrating targeted biomarker profiling into clinical practice to enable personalized, biomarker-informed interventions aimed at restoring fertility and metabolic health in patients with PCOS. - Source: PubMed
Publication date: 2026/06/25
El-Sehrawy Amr Ali Mohamed AbdelgawwadAljumaili Omer IBaig Mirza RNematov OzodbekSapaev Ibrokhim BBadr Istabraq HSmerat AseelBasunduwah Tina Saeed - The aim of the present study was to explore the reparative effects of spermidine combined with umbilical cord mesenchymal stem cells (UC-MSCs) on endometrial injury in mice. First, bioinformatic results suggested that endometrial damage is closely linked to immune mechanisms, a finding that was corroborated by quantitative polymerase chain reaction results. Next, an endometrial injury model was established by injecting 95% ethanol into the uterus, and spermidine combined with UC-MSCs was used for treatment. We found that the combination of spermidine and umbilical cord mesenchymal stem cells (S+UC-MSCs) significantly reduced CD36 expression while significantly increasing the expression of the proteins THBS2, TIMP3, CLU, and CFH. In addition, S + UC-MSCs significantly increased the number of Tregs and the protein levels of interleukin-4 (IL-4) and interleukin-10 (IL-10), whereas the protein levels of interleukin-6 (IL-6), interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α), interleukin-2 (IL-2), and interleukin-17 (IL-17) decreased significantly. Furthermore, S + UC-MSCs also improved the morphology of mouse endometria by regulating angiogenesis (microvessel density [MVD] and vascular endothelial growth factor [VEGF]) and receptivity (HOXA10, LIF, LPAR3, and αvβ3). These results indicated that the combined therapy of spermidine and UC-MSCs promotes angiogenesis, enhances uterine receptivity, regulates the IL-10/Treg-mediated immune microenvironment to restore endometrial morphology, and shows a tendency to increase the pregnancy rate in mice. - Source: PubMed
Publication date: 2026/06/24
Sun KaiheLin XiuyingNiu ChunxueMi XuguangChen ShilingJin Dan - Obesity is recognized as a key contributor to the impaired endometrial receptivity that results in infertility; however, the molecular mechanisms underlying endometrial dysfunction remain incompletely understood. In this study, proteomic and ubiquitination analyses of secretory-phase endometrial tissue revealed a significant upregulation of SNCA/synuclein alpha and dysregulation of macroautophagy/autophagy in women with obesity. SNCA is best known for its role in neurodegenerative protein aggregation disorders. Proteomic and ubiquitination analysis of secretory-phase endometrial tissue revealed a significant upregulation of SNCA and dysregulation of autophagy in women with obesity. This study aimed to elucidate the role and mechanistic basis of SNCA and autophagy in obesity-associated endometrial receptivity defects. We demonstrated that elevated SNCA expression in endometrium and endometrial stromal cells (ESCs) correlated with impaired autophagy and disrupted decidualization in and . Mechanistically, SNCA directly interacted with the E3 ubiquitin ligase STUB1 (STIP1 homology and U-box containing protein 1) in ESCs, thereby disrupting the association between STUB1 and phosphorylated TFEB (transcription factor EB; p-TFEB). This interaction attenuated p‑TFEB degradation, leading to suppressed autophagic flux and ultimately compromised decidualization of ESCs. Conversely, knockout alleviated obesity-induced endometrial impairments in mice. Moreover, STUB1 overexpression rescued decidualization and autophagy defects. Notably, metformin intervention restored autophagic activity and endometrial receptivity in obese mice by downregulation of SNCA independent of its autophagy-modulating effects. Together, these findings uncovered a novel pathogenic mechanism in which obesity-driven SNCA overexpression impairs endometrial receptivity by inhibiting STUB1-TFEB-mediated autophagy, positioning the SNCA-STUB1-TFEB axis as a promising therapeutic target for obesity-related endometrial infertility.: BECN1: beclin 1; CCK-8: Cell Counting Kit-8; CQ: chloroquine; DEPs: differentially expressed proteins; DIO: diet-induced obese; ESCs: endometrial stromal cells; FBS: fetal bovine serum; GD7: gestational day 7; GSEA: Gene Set Enrichment Analysis; HFD: high-fat diet; HOXA10: homeobox A10; IGFBP1: insulin like growth factor binding protein 1; IPGTT: intraperitoneal glucose tolerance test; LIF: LIF interleukin 6 family cytokine; PBS: phosphate-buffered saline; PRL: prolactin; Rapa: rapamycin; SNCA/synuclein alpha; SQSTM1/p62: sequestosome 1; STUB1: STIP1 homology and U-box containing protein 1; TC: total cholesterol; TEM: transmission electron microscopy; TFEB: transcription factor EB; UPS: ubiquitin-proteasome system; WOI: window of implantation. - Source: PubMed
Publication date: 2026/06/23
Tang FeiGuo PeipeiWang LitingXie PengxiangWang YiWang YueFang YouyanLi CaihuaCao YunxiaXiang HuifenYin ZongzhiZhang DongWei ZhaolianHe Ye - Radiation-induced intestinal injury (RIII) represents a significant dose-limiting complication of radiotherapy, characterized by substantial loss of intestinal epithelial cells (IECs). While the activation of cannabinoid receptor 2 (CB2R) is protective in immune‑mediated colitis, the intrinsic role of CB2R in IECs and its potential therapeutic relevance in RIII have not been defined. - Source: PubMed
Publication date: 2026/05/16
Yao QianyiTian YingYuan YiCai YongqingYang QunfangZhang LanfangLi YunongWei TanjunWang YiOuyang QinZhang HaigangLi XiaoliLiu Tao - : Aging is increasingly recognized as a key determinant of changes in human tissue and cellular function. Women's age, in particular, has been associated with reduced oocyte quality and negatively correlated with the expression of genes involved in endometrial decidualization and cellular function. The ability of endometrial cells to interact and allow the invasion of the growing embryo is defined as endometrial receptivity. Investigating age-related differences in human endometrial receptivity may expand our understanding of factors contributing to infertility. : Stromal cells were isolated and cultured from endometrial pipelle biopsies ( = 28) obtained from female donors at the proliferative phase of the menstrual cycle. Protein and mRNA expression of the receptivity modulators OPN, CD44, and HOXA10 were analyzed by Western blot and real-time PCR, respectively. : Data presented a linear decrease in mRNA expression of OPN and HOXA10 ( = 0.0066, R = 0.3018 and = 0.0036, R = 0.529, respectively) with women's increasing age, and a similar trend was evident at the protein level (OPN, < 0.05; HOXA10, < 0.01). Further analysis of the data included separating the samples into three age groups: 25-35 years, 36-40 years, and 41-46 years. ANOVA revealed a significant decrease in OPN and HOXA10 mRNA expression ( = 0.03158 and = 0.02578, respectively). CD44 expression did not differ with age. : OPN and HOXA10 are negatively correlated with increasing maternal age. These findings suggest that age-related alterations in key endometrial receptivity modulators may contribute to impaired implantation and could represent potential targets for diagnostic or therapeutic strategies in human implantation failure. - Source: PubMed
Publication date: 2026/04/29
Makrygiannakis FanouriosMarmara MariaVrekoussis ThomasNikitovic DraganaMakrigiannakis AntoniosBerdiaki Aikaterini