Ask about this productRelated genes to: ALDH1A1 antibody
- Gene:
- ALDH1A1 NIH gene
- Name:
- aldehyde dehydrogenase 1 family member A1
- Previous symbol:
- PUMB1, ALDH1
- Synonyms:
- RALDH1
- Chromosome:
- 9q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2015-11-18
Related products to: ALDH1A1 antibody
Related articles to: ALDH1A1 antibody
- Intrauterine adhesions (IUA), a leading cause of uterine infertility, are characterized by endometrial fibrosis and a loss of functional regeneration. The impairment of endometrial mesenchymal stem/stromal cells (eMSCs) is central to IUA pathogenesis; however, the absence of reliable markers correlating with disease severity and fibrosis has hindered the understanding of their pathological mechanisms and the development of targeted therapies. Here, ALDH1A1 and ALDH1A2 were identified as novel eMSC markers significantly downregulated in IUA patient samples and scar tissue. ALDH eMSCs exhibited superior self-renewal capability, proliferative capacity, decidualization potential, and angiogenic capability, alongside reduced fibrotic characteristics compared to ALDH eMSCs. Transplantation of ALDH eMSCs promoted endometrial regeneration in a murine IUA model. Mechanistically, ALDH eMSCs secreted higher levels of ATRA (all-trans retinoic acid), and their pro-regenerative effect was mediated through the ALDH-RA-RAR (RA Receptor) axis. ATRA and E2 (Estradiol) acted synergistically to promote glandular organoid growth and reprogram ALDH eMSCs towards a regenerative phenotype. The RE-Exo@HA hydrogel, composed of ATRA and E2 encapsulated in exosomes embedded within a hyaluronic acid hydrogel, effectively facilitated scarless endometrial repair, demonstrated by restored endometrial architecture, increased gland number, reduced fibrosis, and significantly improved pregnancy outcomes in vivo. Our findings establish ALDH1A1/ALDH1A2 as key functional markers of a regenerative eMSC subpopulation depleted in IUA and highlight the ALDH-RA axis as a critical mechanism governing endometrial repair. - Source: PubMed
Publication date: 2026/08/25
Chen SiXing ShichaoYuan WenpengWang YueLiu JingqiSong JunLi MeiqiZhang JingtingShi ShaoquanXu Jianyong - Cancer stem cells (CSCs) play a pivotal role in tumor initiation, progression, and therapy resistance. Emerging evidence suggests that non-coding RNAs (ncRNAs), including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), intricately regulate CSC properties. This article reviews current knowledge on the intricate interplay between ncRNAs, genetic and epigenetic factors having role in cancer stemness and associated phenotypes. We have also identified key stemness- and EMT-associated genes, including , , , , , , , , , , , and that are regulated by ncRNAs in different cancer types. Additionally, we have described how ncRNA-mediated regulation of these genes influences major signaling pathways, including Wnt/β-catenin, Notch, Hedgehog, PI3K/AKT/mTOR, JAK/STAT, NF-κB, Hippo/YAP, and TGF-β signaling. The mir-21, miR-34, miR-200, and let-7 families target self-renewal and epithelial-to-mesenchymal transition while lncRNAs like H19, HOTAIR, and MALAT1 remodel the regulatory and epigenetic landscape of cancer stem cells. Understanding the interplay between ncRNAs and CSCs offers new insights into potential targeted therapies for combating aggressive and therapy-resistant cancers. Additionally, combining ncRNA interventions with conventional modalities such as chemotherapy, epigenetic drugs along with the advance nanotechnology-based drug delivery systems could result into synergistic outcomes. However, delivery, efficacy, and safety challenges remain. Overall, the ncRNA-cancer stemness interplay warrants therapeutic advancements and clinical translation towards a promising treatment personalization. - Source: PubMed
Publication date: 2026/08/06
Chen SongDakal Tikam ChandBhushan RaviArya Dilip KumarGogoi BhaskarKumar AbhishekSchmidt-Wolf Ingo G HSharma AmitChen Meiling - Adult stem cells are thought to drive the regenerative potential of the endometrium and contribute to the pathogenesis of endometriosis; however, their identity and defining features remain to be characterized. Here, we used in vivo and in vitro approaches to demonstrate that cells with high aldehyde dehydrogenase 1 activity (ALDH cells) were long-lived progenitors in the endometrium with a higher organoid formation capacity, long-term passaging potential, and stemness gene signatures. Using lineage tracing with an reporter mouse, epithelial cells expanded during postnatal development, stromal cells expanded during estrous cycling, and both populations of cells were present during postpartum repair. In response to ovariectomy or exogenous estradiol, we found that ALDH1A1 cells localized to glandular crypts of the endometrium or throughout the luminal epithelium, respectively, indicating that their spatial localization is hormone-sensitive. Functionally, we found that selective ablation of ALDH1A1 cells in mice decreased endometrial gland number and FOXA2 expression. These findings were recapitulated in the human endometrium, where endometrial epithelial organoids with high ALDH activity (ALDH cells) showed a higher organoid formation capacity than ALDH cells and displayed unique transcriptomes with fewer luminal-like ciliated cells. Overall, our studies indicate that ALDH1A1 cells are hormone-sensitive adult stem cells in the endometrium with regenerative potential that are critical for endometrial development and function. - Source: PubMed
Publication date: 2026/08/06
Tang SuniUnser Anna CatherineJiang PeixinParks Sydney EHerrera Genesis JGeng TingAlpuing Radilla LindaThigpen Brooke AGuan XiaomingMonsivais Diana - Aldehyde dehydrogenase 1A1 (ALDH1A1) has emerged as a promising therapeutic target because of its critical roles in cancer stem cell maintenance and chemoresistance. However, the development of highly selective ALDH1A1 inhibitors remains challenging because of the extensive structural conservation shared with the closely related isoforms ALDH2 and ALDH1A2. In this study, we developed an integrated computer-aided drug design (CADD) and artificial intelligence (AI) framework to systematically identify selective ALDH1A1 inhibitors from a heterocyclic compound library. The multistage virtual screening workflow integrated deep learning-assisted molecular docking, convolutional neural network (CNN)-based scoring, and stringent isoform selectivity filtering. Subsequently, a LightGBM-based classification model was applied to prioritize candidate inhibitors, advancing LDN-27219 and TUG-1375 for dynamic validation. The dynamic stability and binding energetics of the selected protein-ligand complexes were further evaluated using molecular dynamics simulations and molecular mechanics-Poisson-Boltzmann surface area (MM/PBSA) calculations. Collectively, the computational analyses suggest that LDN-27219 exhibits favorable binding characteristics and represents a promising lead candidate for subsequent experimental validation. This integrated AI-CADD framework provides an efficient and reliable strategy for the rapid identification and prioritization of structurally novel, isoform-selective ALDH1A1 inhibitors for future drug discovery efforts. - Source: PubMed
Publication date: 2026/07/30
Cho Shu-ChiWang Yi-WenChu Chien-AnHuang Ming-ChihPangging MonmiLee Chung-Ta - Tubo-ovarian high-grade serous carcinoma (HGSC) has a poor prognosis due to limited treatment options, therapy resistance, and high recurrence rates. One proposed mechanism underlying treatment failure is the survival of cancer stem cells (CSCs) following chemotherapy. In previous in vitro studies, we identified ALDH1A1, SOX2, MYC, and BMI1 as putative CSC markers, with increased expression linked to platinum resistance. This study aimed to evaluate the expression and prognostic relevance of these four markers in diagnostic, treatment-naïve HGSC tissue specimens. - Source: PubMed
Publication date: 2026/07/29
Roering PiaCsellar LillaBlom SamiRaineva IonaColangelo KiaHänninen SatuLaury Anna RayHeuser Vanina DCarpén Olli