Ask about this productRelated 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
- The role of Klotho in heart failure (HF) and its underlying metabolic mechanisms remain unclear. This study investigated how Klotho deficiency affects extracellular matrix (ECM) homeostasis and metabolic regulation in post-myocardial infarction HF (MI-HF), with a focus on aldehyde dehydrogenase 1 family member L1 (ALDH1L1). - Source: PubMed
Publication date: 2026/08/31
Zhao BingXiao Chun - Folic acid (FA) supplementation during pregnancy is the commonly accepted treatment to prevent neural tube defects. The mechanism by which FA prevents neural tube defects (NTDs) remains unclear. FA also prevents other developmental malformations, including alcohol-induced malformations in Fetal Alcohol Syndrome models. We show that FA acts through a metabolic link to retinoic acid (RA) signaling. Using a -knockdown model of FA-rescuable NTDs, we show that RA or its precursors equally rescue these defects. Similarly, FA rescues alcohol-induced NTDs in a model previously shown to be rescued by retinoids. We identify the FA-metabolizing enzyme, formyl tetrahydrofolate dehydrogenase (ALDH1L1, FTHFD), encoded by the gene, as essential for this rescue. Mechanistically, FA upregulates expression, thereby increasing RA biosynthesis. Knockdown of ALDH1L1 activity using CRISPR/Cas9 abolishes the FA protective effect. To support these observations, we show that the human ALDH1L1 enzyme converts retinaldehyde to RA, and its overexpression restores neural tube closure in -knockdown embryos when retinaldehyde is provided. At the cellular level, reduced RA signaling results in overproliferation of neural plate precursors and a pathological expansion of the neural tube. ALDH1L1 enables FA to restore normal neural plate proliferation, thereby preventing NTDs. These findings establish ALDH1L1 as an unexpected enzymatic link between FA (vitamin B9) and RA signaling, revealing how FA supplementation safeguards neural development and suggesting opportunities to refine strategies for NTD prevention. - Source: PubMed
Publication date: 2026/07/30
Edri TamirAbbou-Levy TaliCohen DorInácio José MShabtai YehudaPillemer GracielaBelo José AntónioFainsod Abraham - Intracerebral hemorrhage (ICH) leads to significant neuronal loss and glial scar formation, but the regenerative capacity of the adult brain remains limited. Although small-molecule-induced astrocyte-to-neuron (AtN) conversion has shown promise in vitro, in vivo applications-particularly under pathological conditions-are still scarce. We aimed to develop and validate a small-molecule cocktail for inducing astrocyte-to-neuron reprogramming in vivo following ICH. We identified a seven-compound cocktail (DFGKLRV) capable of converting astrocytes into neurons under both physiological and ICH conditions. Using immunostaining, RT‒qPCR, electrophysiology, RNA sequencing, neural circuit tracing, and behavioral assessment, we assessed the identity and functionality of induced neurons. In vivo reprogramming was achieved via continuous intracerebral infusion of the cocktail using osmotic pumps. Lineage tracing with aldehyde dehydrogenase 1 family member L1 (Aldh1l1)-Cre/Rosa-CAG-tdTomato mice confirmed the astrocytic origin of the reprogrammed neurons. Additionally, we monitored ferroptosis dynamics during reprogramming and evaluated the effect of ferroptosis inhibition on conversion efficiency. DFGKLRV successfully reprogrammed astrocytes into functional, electrophysiologically active neurons. This reprogramming was effective both in vitro and in vivo, including in the hemorrhagic brain environment. Pharmacological inhibition of ferroptosis significantly improved reprogramming efficiency. Mechanistically, ferroptosis inhibition promoted astrocyte-to-neuron conversion at least in part through suppression of the TGF-β/SMAD3/SOX9 axis, whereas exogenous TGF-β1 treatment or Sox9 overexpression reversed this pro-reprogramming effect. Our findings demonstrate that the DFGKLRV cocktail enables efficient in vivo astrocyte-to-neuron reprogramming following ICH. Moreover, ferroptosis represents a key regulatory mechanism and potential therapeutic target for enhancing chemical reprogramming strategies. - Source: PubMed
Publication date: 2026/07/29
Wang JingyiChen ShilingLi JiaruiLiu XiaWang JiahuiHuang LiyangNie LuweiWu XuanLi YunjieFeng YangyangLiu NaTang YingxinZhu LingqiangQin ChuanLi GaigaiTang Zhouping - Peripheral nerve injury (PNI) induces neuroinflammatory responses in the spinal cord that contribute to neuropathic pain. While microglial proliferation is a well-established feature of this process, whether spinal astrocytes undergo proliferation after PNI seems to be controversial. In this study, we examined astrocytic proliferative responses using Aldh1l1-GFP transgenic mice subjected to spinal nerve ligation (SNL), combined with immunohistochemical and transcriptomic analyses. SNL elicited a temporally organized glial reaction, characterized by early microglial reactivity followed by delayed astrocytic reactivity marked by increased GFAP expression. Despite pronounced astrocytic reactivity, the number of Aldh1l1-GFP⁺ astrocytes in the spinal dorsal horn remained unchanged across all examined time points, and only negligible colocalization with proliferation markers (Ki67 and EdU) was detected. Consistently, transcriptomic analyses revealed extensive astrocyte-associated transcriptional reprogramming without activation of cell-cycle gene programs after PNI. Minimally proliferative astrocytic responses were observed in additional cranial nerve injury model, partial infraorbital nerve transection (pIONT), in which proliferative responses in medullary dorsal horn were also restricted to microglia. Together, these findings demonstrate that spinal or medullary astrocytes respond to PNI with minimal proliferation (rare colocalization with proliferation markers) and primarily through reactive remodeling rather than cell division, providing direct evidence addressing previous inconsistencies and highlighting astrocytic functional plasticity as a key mechanism contributing to neuropathic pain. - Source: PubMed
Publication date: 2026/06/29
Deng Yu-TaoLiu Qing-YeZheng Xuan-JieBai Xue-HuiZeng Jie-TingJiang Bao-Chun - Seasonal crude protein (CP) and phosphorus (P) deficiency in northern Australian pastures reduces feed intake and growth of grazing ruminants, but the hepatic mitochondrial mechanisms underlying this response remain unclear. We characterized the hepatic mitochondrial transcriptome of sheep exposed to CP-P deficiency or matched-intake feed restriction. Merino wethers were assigned for 63 d to one of three treatments ( = 8/group): High CP-P, Low CP-P, or Restricted, in which High CP-P feed was offered at the same energy intake as the Low CP-P group. Liver RNA was sequenced, and transcripts encoding mitochondrial proteins were identified using MitoCarta 3.0. Differentially expressed genes (DEGs) were defined as adjusted < 0.05 and |log2FC| ≥ 0.585. Of 804 mitochondrial genes detected, 83 were differentially expressed in at least one pairwise comparison. The greatest transcriptional response occurred in contrasts against High CP-P (Low CP-P vs. High CP-P: 38 DEGs in 8 enriched pathways; Restricted vs. High CP-P: 37 DEGs in 10 enriched pathways). In both low-intake treatments, , , , and were upregulated, suggesting altered folate-mediated one-carbon metabolism. Restricted sheep also showed higher expression of several transporters (, , , , and ), indicative of enhanced mitochondrial nucleotide and metabolite exchange under CP-P adequate energy restriction. In contrast, Low CP-P sheep showed higher expression of and relative to either High CP-P or Restricted sheep, a nutrient-deficiency specific transporter response. expression was also higher in Restricted sheep than in both other groups. These findings suggest that reduced metabolizable energy intake was associated with the bulk of the hepatic mitochondrial transcriptional response, particularly in folate-mediated one-carbon metabolism, whereas CP-P deficiency was associated with a smaller but distinct transporter signature. The liver mitochondrial transcriptome may provide mechanistic insight into nutritional adaptation under CP and P deficiency in grazing sheep. - Source: PubMed
Publication date: 2026/05/31
Fernandez Elmer EInnes David JBottje Walter GFortes Marina R SPoppi Dennis PQuigley Simon PBond Jude JHudson Nicholas J