ALDH1L1 antibody
- Known as:
- ALDH1L1 (anti-)
- Catalog number:
- orb101820
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- ALDH1L1 antibody
Related genes to: ALDH1L1 antibody
- Gene:
- ALDH1L1 NIH gene
- Name:
- aldehyde dehydrogenase 1 family member L1
- Previous symbol:
- FTHFD
- Synonyms:
- 10-fTHF, FDH
- Chromosome:
- 3q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-23
- Date modifiied:
- 2019-01-11
Related products to: ALDH1L1 antibody
Related articles to: ALDH1L1 antibody
- ALDH1L1, a key enzyme in folate metabolism, has been implicated in various cancers, but the clinical significance of its expression in breast cancer remains unclear. - Source: PubMed
Publication date: 2026/05/25
Ryu Han SukAbdellatef Amira AKim Da SolNikas Ilias PKrupenko Sergey A - Astrocytes play vital roles in regulating brain states across organisms. Specifically, they regulate breathing behaviors and associated brain states, including facilitating transitions between breathing phases by sensing changes in O₂ and CO₂ levels, regulating the sleep-wake cycle, and impacting arousal and wakefulness. Here, we test the hypothesis that astrocytes in the ventral respiratory column (VRC) are important for arousal and sigh generation in alert mice. Our results reveal that a subset of Aldh1l1 cells in the VRC are activated prior to sigh generation and are recruited by hypoxia. Chemogenetic or optogenetic activation of Aldh1l1 astrocytes in the VRC increased the probability of evoking arousals with sighs. We also demonstrated that activating Aldh1l1 astrocytes increased calcium transients in catecholaminergic neurons in the VRC immediately before arousal with sighs. We conclude that medullary astrocytes can modulate sigh generation and arousal transitions, and are important for the ventilatory and arousal response to hypoxia. - Source: PubMed
Publication date: 2026/05/23
Oliveira Luiz MarceloMiranda Nicole CastroLim Hyun-KyoungSevers LizaTakakura Ana CarolinaMoreira Thiago SantosLi LiKalume FranckRamirez Jan-Marino - Astrocytes play essential roles in maintaining brain homeostasis and in contributing to synaptic functions, but, in response to injury, infection, or disease, astrocytes can downregulate their homeostatic and physiological functions while increasing neuroinflammatory responses. The central amygdala (CeA) is important for stress responsivity and the development of alcohol (ethanol) dependence. Using a multi-omics approach in Aldh1l1-EGFP/Rpl10a mice and the chronic intermittent ethanol two-bottle choice (CIE-2BC) model, we have characterized the translational response of CeA astrocytes, as well as the proteomic and phosphoproteomic changes in ethanol dependent, non-dependent, and naïve mice. We identified astrocyte-specific alterations in neuroimmune functions and antioxidant/oxidative stress pathways in ethanol dependent mice as well as cytoskeletal plasticity related pathways in non-dependent mice. Proteomic analysis showed down-regulation of astrocyte physiological functions in dependent animals while phosphoproteomic analysis identified pathways associated with cytoskeleton remodeling in both dependent and non-dependent mice. Reconstructions of astrocyte morphologies demonstrated increased CeA astrocyte complexity in dependent and non-dependent groups compared to naïve mice. The astrocyte-specific activation of neuroimmune and antioxidant pathways, down-regulation of homeostatic functions, alteration in protein phosphorylation-mediated cytoskeleton remodeling, and increased astrocyte morphological complexity demonstrate that ethanol dependence induces astrocyte reactivity in the CeA consistent with both adaptive and maladaptive changes. These findings highlight the role of CeA astrocytes in the progression from alcohol intake to dependence and represent a first step toward identifying astrocyte-specific therapeutic strategies to treat Alcohol Use Disorder (AUD) aimed at potentiating reactive astrocyte adaptive changes and inhibiting maladaptive responses. - Source: PubMed
Publication date: 2026/05/22
Hashimoto Joel GGonzalez Angela EGorham NatalieBarbour ZoeRoberts Amanda JDay Le ZNedelescu HerminaHeal MaciDavis Brett ACarbone LuciaJacobs JonRoberto MarisaGuizzetti Marina - Extracellular vesicles (EVs) mediate intercellular transfer of lipids, proteins, and nucleic acids between nearly all cell types. We previously showed that astrocyte-derived EVs modulate neuronal mitochondria , but whether endogenous astrocytic EVs are trafficked to neuronal mitochondria remained unknown. To address this, we generated an EV reporter mouse, Aldh1l1-Cre; CD9-tGFP, in which astrocyte-secreted EVs are labeled with a CD9-turboGFP fusion protein (CD9-tGFP). Astrocyte-specific expression of CD9-tGFP was verified in brain tissue and isolated EVs, comprising 13.2 ± 1.6% of total brain EVs. In primary glial cultures, CD9-tGFP was restricted to astrocytes, localizing to vesicular compartments and cell protrusions (filopodia and cilia), with 89.3 ± 2.2% of astrocyte-derived EVs carrying the label. These EVs were enriched with the sphingolipid ceramide, consistent with its co-distribution with CD9-tGFP in astrocytic cell protrusions. In the cortex, hippocampus, and cerebellum, CD9-tGFP was predominantly detected in astrocytic processes co-labeled with GLAST1 and GFAP, forming contacts with laminin-positive capillaries and parvalbumin-positive neurons. CD9-tGFP-labeled EVs were detected inside capillaries and neurons, and super-resolution STED microscopy revealed partial overlap with neuronal mitochondria. Live-cell spinning disk confocal imaging and AI-assisted proximity analysis confirmed uptake of CD9-tGFP EVs by neuronal cells and trafficking of their cargo to mitochondria . Biochemical isolation of synaptic and non-synaptic mitochondria confirmed EV-derived cargo on mitochondria , with 3-fold higher association of CD9-tGFP with synaptic than non-synaptic mitochondria. Together, these findings validate the Aldh1l1-Cre; CD9-tGFP reporter mouse as a powerful tool for tracking astrocyte-derived EVs and provide direct evidence that their cargo is preferentially trafficked to synaptic mitochondria. - Source: PubMed
Publication date: 2026/04/21
Ren XiaojiaQuadri ZainuddinZhu ZhihuiFu XuZhang LipingBieberich Erhard - Although there are several proteomic studies testing brain responses to glucocorticoids, there were no attempts to integrate these data and compare them with responses at the level of mRNAs. Furthermore, the utility of available data is compromised by changes in nomenclature and usage of different types of identifiers. Therefore, the aim of this study was to identify the most consistent changes in protein expression in standardized mouse, rat, and human datasets and compare them with transcriptomic responses to glucocorticoids. The analysis showed that the two most frequently and consistently detected proteins were ATP synthase F1 subunit beta (Atp5f1b) and aldolase, fructose-bisphosphate C (Aldoc), while the most consistent proteomic and transcriptomic findings included Aldoc, Plin4, Aqp4, Endod1, Glul, Anln, Aldh1l1, Parp1, Trf, Fermt2, Tmem63a, and Trim2. The study also revealed limitations of available proteomic data indicating significant gaps in knowledge. Finally, the study provides an integrated dataset with updated protein nomenclature and a complete set of major identifiers to facilitate usage of proteomic data. - Source: PubMed
Juszczak Grzegorz R