ALDH1A1 (Internal) Antibody
- Known as:
- ALDH1A1 (Internal) Antibody
- Catalog number:
- AF1051b
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ALDH1A1 (Internal) Antibody
Related genes to: ALDH1A1 (Internal) 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 (Internal) Antibody
Related articles to: ALDH1A1 (Internal) Antibody
- 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 - Extracellular vesicles (EVs) mediate intercellular transfer of lipids, proteins, and nucleic acids between cell types. We previously showed that astrocyte-derived EVs modulate neuronal mitochondria in vitro. Whether endogenous astrocytic EVs associate with neuronal mitochondria in vivo remained unknown. To address this, we generated an EV reporter mouse, Aldh1l1-Cre; CD9-tGFP, which resulted in fluorescent labeling of astrocyte-derived CD9-positive EVs. Astrocyte-specific expression of CD9-tGFP was verified in brain tissue, where CD9-tGFP-positive particles comprised 13.2% ± 1.6% of total isolated EVs. In primary glial cultures, CD9-tGFP was restricted to astrocytes, localizing to vesicular compartments and cell protrusions (filopodia and cilia); 89.3% ± 2.2% of astrocyte-derived EVs were CD9-tGFP positive. In cortex, hippocampus, and cerebellum, CD9-tGFP was predominantly detected in astrocytic processes co-labeled with glutamate aspartate transporter 1 (GLAST1) and glial fibrillary acidic protein (GFAP), forming contacts with laminin-positive capillaries and parvalbumin-positive neurons. CD9-tGFP-labeled EVs were detected at capillaries and inside neurons, and STED microscopy revealed partial co-localization with neuronal mitochondria. Live-cell spinning disk confocal imaging and AI-assisted proximity analysis confirmed uptake of CD9-tGFP EVs by neuronal cells and cargo enrichment at mitochondria in vitro. Immunoblotting and imaging of isolated mitochondria established physical association with EV-derived CD9-tGFP in vivo, with 3-fold higher CD9-tGFP puncta density on synaptic mitochondria. Together, these findings validate the Aldh1l1-Cre; CD9-tGFP reporter mouse as a tool for tracking astrocyte-derived EVs in vivo and provide evidence of preferential cargo enrichment at synaptic mitochondria. - Source: PubMed
Ren XiaojiaQuadri ZainuddinZhu ZhihuiFu XuZhang LipingBieberich Erhard - Recent studies have implicated dopaminergic signaling within the substantia nigra pars reticulata (SNr) in the emergence of Parkinsonian motor deficits. To better understand the mechanisms underlying this dependence, the ability of dopamine to modulate SNr neuron activity was studied in ex vivo mouse brain slices. In addition to presynaptically inhibiting phasic GABA release, D2 dopamine receptor (D2R) signaling unexpectedly suppressed a tonic, GABA receptor-mediated inhibition of SNr neuron spiking. Our studies demonstrated that this tonic modulation was largely mediated by GAT-1-dependent GABA release from ALDH1A1-expressing dopaminergic neurons. In contrast, the ability of D2R agonists to disinhibit SNr neurons depended on D2R-expressing astrocytes and stimulation of GAT-3 uptake of GABA from the extracellular space. In addition to underscoring the importance of dendritically released dopamine in modulating synaptic transmission, our studies demonstrate that dopaminergic modulation of astrocytes plays a key role in modulating SNr circuits and motor behavior. - Source: PubMed
Publication date: 2026/09/09
Simmons DeNard VMoreno-Ramos Oscar AndrésRaj Divya D AKaganovsky KonstantinPamukcu ArinVrieler NoraTkatch TatianaXie Zhongde Sousa Ana Isabel SilvaZampese EnricoDing JunAwatramani RajeshwarWilson Charles JSurmeier D James