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
- Low birthweight increases chronic kidney disease (CKD) risk. Using a gestational low protein (LP) mouse model, we hypothesized that protein restriction would alter nephrogenesis and adult gene expression. Pregnant CD-1 dams received normal protein (NP) or LP diets. Pups were studied on postnatal days 2-7 to assess the nephron progenitor cell population. Adult mice underwent transdermal GFR measurement and histologic evaluation, bulk RNA sequencing, and cationic-ferritin-enhanced MRI. Nephrogenesis was protracted in LP mice compared with NP mice. Adult LP mice had fewer glomeruli. LP males had lower GFR and more atubular glomeruli without glomerular hypertrophy. LP males demonstrated down-regulated and LP females demonstrated down-regulation. LP offspring exhibited prolonged postnatal nephrogenesis with a lower glomerular number as adults, indicating an extended developmental window did not compensate for their reduced nephron endowment at birth. Suppression of the retinoic acid-GDNF signaling pathway was present in LP males. These findings identify a potential early life therapeutic window to mitigate CKD risk in growth-restricted offspring. - Source: PubMed
Publication date: 2026/09/23
Timberline SageDailey Rachel KJohnson WyattKameshwar Ayyappa Kumar SistaIsaac JayadeRonde KimberlyConaway MarkCwiek AleksandraBennett Kevin MBaldelomar Edwin JLi TengWu TeresaHoch Matthew RSchuh Meredith PIndugula ShaliniSeki YoshinoriSuzuki MasakoReidy Kimberly JCharlton Jennifer R - Head and neck squamous cell carcinoma (HNSCC) remains a leading cause of cancer mortality worldwide, with treatment resistance posing a major clinical challenge. The tumor microenvironment, particularly the three-dimensional (3D) extracellular matrix architecture, plays a critical role in driving therapy resistance, yet the underlying molecular mechanisms remain incompletely understood. Here we investigate how the 3D collagen microenvironment orchestrates chemoresistance through NF-κB/STAT3 signaling and partial epithelial-mesenchymal transition (EMT) in HNSCC. Using 3D type I collagen culture systems, both FaDu and CAL27 HNSCC cells form spheroidal structures with cytoskeletal reorganization. Compared to 2D monolayers, 3D collagen culture activated NF-κB signaling, upregulated stemness marker ALDH1A1 and drug resistance proteins ABCG2/Bcl2, and significantly increased IC50 values for paclitaxel and cisplatin in FaDu and CAL27 cells. NF-κB inhibitor PDTC reversed these phenotypes, reducing resistance marker expression and restoring chemosensitivity. In FaDu xenografts, PDTC combined with paclitaxel exerted enhanced antitumor effects, achieving greatest tumor growth inhibition. Mechanistically, we identified a signaling hierarchy with NF-κB upstream of STAT3; PDTC suppressed both pathways, while Stat3 inhibitor Stattic only affected STAT3 downstream effectors. Clinical relevance was confirmed by immunohistochemistry of human HNSCC specimens, showing spatial enrichment of p65/p-p65 at the tumor-stroma interface specifically in lymph node-positive cases, with p-p65 H-scores significantly higher in metastatic patients (p < 0.05). Importantly, 3D collagen induced a partial EMT state with concurrent E-cadherin and N-cadherin upregulation, downregulation of ZO-1 and upregulation of Slug. Using a 14-gene p-EMT score in chemoresistant patient data, RELA and STAT3 strongly correlated with this hybrid score (RELA: R = 0.75; STAT3: R = 0.82) and activated mesenchymal genes while preserving epithelial identity. These findings demonstrate that the 3D collagen microenvironment activates an NF-κB-Stat3 signaling axis that drives cancer stemness, p-EMT, and chemoresistance in HNSCC, highlighting NF-κB inhibition as a promising therapeutic strategy to overcome microenvironment-mediated resistance. - Source: PubMed
Gu CuirongLi LongGan YuxinLiu HuifenWan YuanLi DongxuMi Kun - Retinoids (i.e., vitamin A and metabolites) have biological importance for functions involved in growth and development, immunity, and reproduction. Previous studies involving retinoids have demonstrated positive associations with increased luteal progesterone (P4) concentrations, and similarly, progesterone has been implicated in the regulation of uterine secretion of retinol-binding protein (RBP), warranting further investigation. Therefore, the aim of this study was to identify the expression of various enzymes and binding proteins involved in vitamin A metabolism in corpora lutea (CL) and endometria during day 15 of the estrous cycle and throughout various points of gestation in gilts. Sexually mature, crossbred gilts were ovariohysterectomized on days 11, 15, 60, or 90 of pregnancy, or day 15 of the estrous cycle (cyclic day 15). Plasma was collected for P4 and vitamin A analysis. Corpora luteal and endometrial tissues were analyzed for mRNAs associated with vitamin A metabolism. There were no differences in CL count, P4 concentrations, or vitamin A concentrations by cyclic or gestational day (P > 0.05). Corpora lutea expression of aldehyde dehydrogenase 1 family member A1 (ALDH1A1) and RBP4 mRNAs were greater on day 15 of pregnancy compared cyclic day 15 gilts (P < 0.05). Moreover, corpora lutea mRNA expression of ALDH1A1 (P = 0.0003), RBP2 (P = 0.02), and alcohol dehydrogenase 1C (ADH1C, P = 0.07) were greater on day 11 of pregnancy. Corpora lutea expression of lecithin retinol acyltransferase (LRAT) mRNA were not different (P > 0.05). Endometrial mRNA expression of ALDH1A1 was greater on cyclic day 15 compared to day 15 of pregnancy (P = 0.002). Endometrial mRNA expression of ALDH1A1 and LRAT were greater on days 60 and 90 of pregnancy compared to days 11 and 15 of pregnancy (P ≤ 0.0001). Endometrial expression of RBP4 mRNA was greater on days 11 and 60 compared to day 90, and greater on day 60 compared to day 15 (P = 0.01). Endometrial expression of ADH1C and RBP2 mRNAs were not different (P > 0.05). These results suggest that genes encoding enzymes involved in vitamin A metabolism (ALDH1A1, ADH1C, RBP2, and RBP4) are elevated in the CL during the period of early gestation when the anti-luteolytic mechanism of maternal recognition of pregnancy is occurring. Additionally, certain genes encoding enzymes involved in vitamin A metabolism (ALDH1A1 and LRAT) are elevated mid- to late-gestation in the endometrium of pregnant pigs. - Source: PubMed
Publication date: 2026/09/18
Stuehr Matthew DHickman Kyle JWiegert Jeffrey GPoole Rebecca K - Epigenetic modifier factors in B cell lymphomas often harbor loss-of-function mutations. Mutations occurring in the histone-lysine methyltransferase 2D (KMT2D) gene are the pivotal chromatin-modifying hallmarks of follicular lymphoma (FL) subsets, however their tumor-promoting roles are unclear. - Source: PubMed
Publication date: 2026/09/15
Zhu YuqianYao JingweiJiang YuelongLai QianChen QinweiZhang JingxingDeng ManmanLin ZhijuanLuo YimingLi ZhifengLiu LongZheng ZhongZha JieXu Bing - Metastasis, chemoresistance, and tumour recurrence are facilitated by cancer stem cells (CSCs), a small subpopulation of cells capable of regenerating a primary tumour while maintaining the tumour's genetic and phenotypic features. CSCs can be identified by the expression of specific markers; however, the CSC population in ovarian clear cell carcinoma (OCCC), a rare histotype of ovarian cancer, remains poorly defined. Given the well-established role that CSCs play in cancer progression and metastasis, it is critical to identify reliable markers of CSCs in OCCC. Here, we endeavoured to determine whether ALDH1 expression could be used to define OCCC stem cells in OCCC cell lines using a variety of methods including assessing ALDH1A1 expression in spheroids generated under distinct conditions. We also generated and used chemo-resistant cell lines to assess the enrichment of cancer stem cells. Human OCCC cell lines were enriched for CSCs using selective culture conditions and drug resistance methods. CSC-enriched spheroids demonstrated increased expression of stemness markers NANOG and SOX2, while ALDH1A1 expression was enriched only in drug-resistant cell lines, relative to parental cell lines. RNA-seq analyses of CSC-media-derived spheroids versus standard media spheroids provided novel data supporting CSC enrichment and identified transcription factors induced by CSC media. These findings highlight the ambiguous role of ALDH1A1 as a CSC marker in OCCC and demonstrates the utility of CSC enrichment methods for identifying CSC populations in OCCC cell lines. - Source: PubMed
Publication date: 2026/08/22
Gebreyes BlaneKolendowski BartRamos-Valdes YudithShepherd Trevor GDiMattia Gabriel E