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
- During the practice of diagnostic pathology, we identified a case of invasive ductal carcinoma (IDC) of the breast with lung metastases exhibiting a ductal carcinoma in situ (DCIS)-like morphology. Immunohistochemistry confirmed the presence of CK5/6, P40 and P63-positive tumor cells at the periphery of the metastatic nests. Subsequent expansion of our sample revealed similar DCIS-like morphology in lymph node metastases of other IDC cases. This study aimed to preliminarily characterize the pathological features, significance, and mechanisms of this phenomenon. - Source: PubMed
Publication date: 2026/09/30
Lin XinFan MingmeiLiu JingquanLong TingGao LingfangWu HaibinZhong YanLin WenwenWang RuianLi ZuguoChen Meihua - The etiology of Parkinson's disease (PD) is associated with exposure to environmental contaminants, including the organochlorine pesticide dieldrin. This is thought to occur through induction of oxidative damage and dysregulation of dopamine homeostasis via impairment of aldehyde dehydrogenase (ALDH) enzymes, resulting in neuronal stress that may contribute to glial-mediated neurotoxicity. We postulated that sub-chronic murine dieldrin exposure would induce PD-relevant histopathologic changes in the substantia nigra (SN) which would be exacerbated in ALDH-deficient mice. To test this hypothesis, six-month-old wildtype and Aldh1a1 X Aldh2 (Aldh1/2 KO) mice were fed dieldrin in chow at doses of 0, 0.2, or 0.6ppm for 6 weeks. Slide scanning microscopy and deep learning-based image analysis were then applied to quantify neuronal injury and glial morphometry. Dieldrin exposure resulted in male-specific dopaminergic neurodegeneration, a dose-dependent increase in astrocytic density, and disease-associated alterations in microglial morphology in the substantia nigra. Interestingly, Aldh1/2 KO attenuated neuronal loss and distinctly modulated reactive astrocytosis and microglial morphometric changes. These results highlight a sex-dependent susceptibility to dieldrin-induced neurotoxicity and suggest a role of ALDH in modulating glial reactivity in the context of PD-like neurodegeneration. - Source: PubMed
Publication date: 2026/09/15
Yanouri Omar ASchuller Adam JRocha Savannah MBriggs Aidan MMartinez Paul AFernandez ElizabethStrong RandyLi XueshuLehmler Hans-JoachimDoorn Jonathan ATjalkens Ronald B - 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