Human Retinal dehydrogenase 1,ALDH1A1 ELISA Kit
- Known as:
- Human Retinal dehydrogenase 1,ALDH1A1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E3259Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- JING
- Gene target:
- Human Retinal dehydrogenase 1 ALDH1A1 ELISA Kit
Ask about this productRelated genes to: Human Retinal dehydrogenase 1,ALDH1A1 ELISA Kit
- 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: Human Retinal dehydrogenase 1,ALDH1A1 ELISA Kit
Related articles to: Human Retinal dehydrogenase 1,ALDH1A1 ELISA Kit
- 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 - To investigate the transcriptional profiling of ocular surface ectoderm (OSE) derived from human embryonic stem cells (hESC), and identified CACNG6 and AQP3 as the surface markers of OSE. - Source: PubMed
Publication date: 2026/08/18
Sun LuLi Yu-MingSong Yu-WenYang Yi-ChenDuan LianGao YangLi Jian-XinYu Yan-KunPang Kun-PengDang Guang-FuZhang Can-Wei - Cerebral venous sinus thrombosis (CVST) is a critical cause of brain injury and intracranial hypertension. However, its underlying molecular mechanisms remain poorly understood, limiting the development of targeted therapies. This study aims to systematically identify key molecular targets and signaling pathways involved in CVST-induced brain lesions using multi-omics approaches in a modified rat model of CVST. An optimized rat CVST model was established. Cortical tissues were collected from Sham-operated, 2-day post-CVST, and 7-day post-CVST groups for transcriptomic, proteomic, and single-cell transcriptomic sequencing. Bioinformatics analyses were performed to identify differentially expressed genes/proteins, followed by functional enrichment, protein-protein interaction network construction, and hub-gene screening. Further investigations included drug enrichment analysis, molecular docking, and molecular dynamics, as well as the prediction of competing endogenous RNA networks, transcription factor analysis, and expression profiling of potential edema-related therapeutic targets. Multi-omics analyses revealed dynamic changes in gene and protein expression in the brain after CVST, along with associated pathways involved in immune inflammatory responses and tissue repair. Integrative analysis identified 12 core genes (, , , , , , , , , , , and ). Single-cell RNA sequencing validated their expression and delineated cell-type specificity. Molecular docking hinted at the high binding potential of glucocorticoids such as dexamethasone and methylprednisolone to several core targets (, , and ), with all docked complexes showing binding energies below -8.2 kcal/mol. Further molecular dynamics simulations indicated that methylprednisolone forms a stable complex with CD44, driven primarily by van der Waals and electrostatic interactions. Additionally, dynamic levels of several potential edema-related targets (, , , and ) were observed. In summary, by applying integrated multi-omics profiling to a modified rat model, this study systematically mapped the molecular landscape of CVST-induced brain injury. A number of candidate targets and signaling pathways emerged from our analysis, along with several compounds of potential therapeutic interest. Collectively, these results provide a basis for further investigation into the mechanisms underlying CVST and for the design of novel treatment approaches. - Source: PubMed
Publication date: 2026/07/16
Qin XiaohongLu HaoranChen ZhibiaoWang YuxuanChen JiangLiu XizhiZhao ZilongZhou JiaqiTian ShuyueDing Rui