Affinage

AARS1

Alanine--tRNA ligase, cytoplasmic · UniProt P49588

Length
968 aa
Mass
106.8 kDa
Annotated
2026-06-09
46 papers in source corpus 23 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

AARS1 is a bifunctional protein that couples canonical protein synthesis to lactate-driven signaling and epigenetic control (PMID:38653238, PMID:39322678, PMID:38512451). In its housekeeping role it is an alanyl-tRNA synthetase whose active site has an inherent amino-acid recognition dilemma: an acidic residue that pins the alpha-amino group of alanine also engages the serine hydroxyl, accounting for serine misactivation, which is corrected by an editing function and backed up cellularly by the independent deacylase DTD that clears mischarged Gly-tRNA-Ala (PMID:20010690, PMID:28362257). The C-terminal C-Ala domain has been structurally repurposed in humans to form a dimer interface with a DNA-binding groove (PMID:27911835). Beyond aminoacylation, AARS1 acts as an intracellular lactate sensor and lactyltransferase, binding lactate with micromolar affinity and catalyzing ATP-dependent formation of lactyl-AMP that is transferred to lysine residues on diverse substrates (PMID:38653238, PMID:39322678, PMID:38512451); the same active-site pocket underlies both serine misactivation and lactyltransferase activity (PMID:40479712). Through this activity AARS1 lactylates p53 in its DNA-binding domain to block its phase separation, DNA binding, and transactivation (PMID:38653238), translocates to the nucleus to lactylate and activate the YAP-TEAD complex in a Hippo-pathway feedback loop (PMID:38512451), and modifies a broad substrate set—including histone H3K18, STAT1, BLM, Akt, NF-kB/p65, and Osterix—thereby linking lactate metabolism to immune signaling, DNA repair, autophagy, and transcriptional programs in cancer and metabolic disease (PMID:40634292, PMID:40987895, PMID:41832952, PMID:40505545). AARS1 mutations cause peripheral neuropathy (CMT2N) through both loss-of-function alleles that reduce tRNA charging and gain-of-function alleles, with certain CMT2N mutations inducing structural loosening of the aminoacylation domain that enables aberrant binding to neuropilin 1 (PMID:22009580, PMID:33753480, PMID:30124830); additional loss-of-function variants underlie trichothiodystrophy, myeloneuropathy, and recurrent acute liver failure (PMID:33909043, PMID:25904691, PMID:33294374).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2009 High

    Established the structural basis for why alanyl-tRNA synthetase misactivates serine, defining the inherent fidelity problem the enzyme must solve.

    Evidence Nine X-ray crystal structures with kinetic and mutational analysis of AlaRS

    PMID:20010690

    Open questions at the time
    • Does not address how misactivation is resolved in vivo beyond the intrinsic editing site
    • Bacterial/structural focus, human-specific differences not resolved
  2. 2011 High

    Showed that a CMT2N disease mutation directly impairs the core aminoacylation function, linking peripheral neuropathy to loss of tRNA charging.

    Evidence In vitro aminoacylation assay and yeast complementation of p.Arg329His

    PMID:22009580

    Open questions at the time
    • Does not explain tissue-specific neuronal vulnerability
    • Later work showed R329H is aminoacylation-normal as purified protein, complicating the loss-of-function model
  3. 2016 High

    Revealed that the C-Ala domain has been repurposed in humans into a DNA-binding module, hinting at non-canonical functions beyond translation.

    Evidence Crystal structures of human C-Ala plus in vitro DNA binding assay

    PMID:27911835

    Open questions at the time
    • Cellular role of C-Ala DNA binding not established
    • No in vivo phenotype tied to this activity
  4. 2017 High

    Defined a secondary cellular checkpoint for AlaRS mischarging errors, showing fidelity depends on a trans-acting deacylase beyond the synthetase's own editing.

    Evidence In vitro deacylation kinetics and genetic epistasis of DTD knockout in an AlaRS editing-defective E. coli background

    PMID:28362257

    Open questions at the time
    • Demonstrated in bacteria; human DTD-AARS1 interplay not directly tested
    • Does not address glycine vs serine error rates in human cells
  5. 2018 High

    Resolved that CMT2N includes both hypomorphic and hypermorphic alleles and that a structural-loosening mechanism enables an aberrant gain-of-function interaction with neuropilin 1.

    Evidence Yeast complementation, aminoacylation assays, zebrafish models, plus biophysical/structural mapping and patient-cell Co-IP of the AlaRS-Nrp1 interaction

    PMID:30124830 PMID:30261202 PMID:33753480

    Open questions at the time
    • How Nrp1 binding causes neurodegeneration mechanistically is unresolved
    • Relationship between mislocalization, gain-of-function binding, and charging defects not unified
  6. 2024 High

    Discovered the moonlighting function: AARS1 is a lactate sensor and lactyltransferase that forms lactyl-AMP and transfers lactyl groups to lysines, redirecting lactate metabolism into signaling and epigenetic regulation.

    Evidence In vitro enzymatic reconstitution of lactylation, lactate binding assays, and proteomics, replicated across labs; genetic code expansion and knock-in mice for the paralogous mechanism

    PMID:38512451 PMID:38653238 PMID:39322678

    Open questions at the time
    • Full substrate repertoire and selectivity rules not defined
    • Regulation of nuclear translocation versus cytoplasmic charging not resolved
  7. 2024 High

    Connected AARS1 lactyltransferase activity to specific transcriptional outputs by showing lactylation inactivates p53 and activates YAP-TEAD in a Hippo feedback loop.

    Evidence Constitutively lactylated p53 variants with DNA-binding and phase-separation assays; nuclear translocation imaging, reporter assays, and loss-of-function in gastric cancer cells

    PMID:38512451 PMID:38653238

    Open questions at the time
    • Stoichiometry of endogenous lactylation on these targets not quantified
    • Whether p53 and YAP-TEAD effects co-occur in the same tumors is untested
  8. 2025 Medium

    Expanded the lactylation substrate network into DNA repair, immune signaling, lipid metabolism, and transcription, establishing AARS1 as a broad metabolic-signaling hub in disease.

    Evidence Co-IP, lactylome/mass spectrometry, site-directed lysine mutations, ubiquitination assays, and conditional knockout mouse models across BLM, STAT1/H3K18, Akt/p65, and Osterix

    PMID:40505545 PMID:40634292 PMID:40987895 PMID:41832952 PMID:42215867

    Open questions at the time
    • Most substrate links rest on single-lab studies
    • Direct versus indirect lactylation not always distinguished from cellular lactate effects
  9. 2025 Medium

    Mapped the mechanistic link between the lactate-binding pocket and serine misactivation, showing a single residue change abolishes both activities.

    Evidence Crystal structure of a pre-activation state plus aminoacylation and lactyltransferase kinetics of an L219M mutant in a bacterial AlaRS ortholog

    PMID:40479712

    Open questions at the time
    • Bacterial ortholog; human pocket equivalence inferred not proven
    • Does not establish physiological lactyltransferase regulation in human cells
  10. 2025 Medium

    Systematically classified recessive AARS1 disease variants and revealed that some can act dominant-negatively, refining genotype-phenotype models.

    Evidence Side-by-side humanized yeast complementation of reported variants with dominant-negative testing (preprint)

    PMID:38979321

    Open questions at the time
    • Preprint, single lab
    • Yeast does not capture human neuronal or lactyltransferase phenotypes

Open questions

Synthesis pass · forward-looking unresolved questions
  • How AARS1 partitions between aminoacylation and lactyltransferase functions, and what controls its nuclear translocation and substrate selection in different tissues, remains unresolved.
  • No unified model linking charging defects, Nrp1 gain-of-function, and lactylation in CMT2N
  • Endogenous lactylation stoichiometry and physiological triggers undefined
  • Substrate specificity determinants of the lactyltransferase activity unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 4 GO:0016874 ligase activity 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0140098 catalytic activity, acting on RNA 3 GO:0003723 RNA binding 2 GO:0140299 molecular sensor activity 2 GO:0140657 ATP-dependent activity 2 GO:0003677 DNA binding 1
Localization
GO:0005634 nucleus 1 GO:0005764 lysosome 1 GO:0005829 cytosol 1
Pathway
R-HSA-1643685 Disease 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-1430728 Metabolism 2 R-HSA-168256 Immune System 2 R-HSA-73894 DNA Repair 1
Partners
AKT1BLMNRP1RELASTAT1TEADYAP1

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2024 AARS1 functions as a lactate sensor that binds lactate with micromolar affinity and catalyzes ATP-dependent formation of lactyl-AMP, which is then transferred to lysine acceptor residues on target proteins, establishing AARS1 as a bona fide lactyltransferase enzyme. In vitro biochemical assay (ATP-dependent lactylation), binding assays, proteomics Cell High 38512451 38653238 39322678
2024 AARS1 lactylates p53 at lysine 120 and lysine 139 in the DNA-binding domain, hindering p53 liquid-liquid phase separation, DNA binding, and transcriptional activation, as demonstrated using constitutively lactylated p53 variants. Proteomics, generation of constitutively lactylated lysine variants, in vitro DNA binding assays, phase separation assays Cell High 38653238
2024 AARS2 (the mitochondrial paralog) associates with cGAS and mediates its lactylation; lactylation at a specific N-terminal site abolishes cGAS liquid-like phase separation and DNA sensing in vitro and in vivo, as confirmed by a genetic code expansion lactyl-lysine incorporation system and knock-in mice. Co-immunoprecipitation, genetic code expansion (orthogonal system for lactyl-lysine incorporation), knock-in mouse models, in vitro phase separation assays Nature High 39322678
2024 AARS1 senses intracellular lactate and translocates into the nucleus, where it lactylates and activates the YAP-TEAD complex; AARS1 itself is a Hippo target gene forming a positive-feedback loop with YAP-TEAD to promote gastric cancer cell proliferation. In vitro lactyltransferase assay, nuclear translocation imaging, reporter assays, loss-of-function studies The Journal of clinical investigation High 38512451
2011 The CMT2N disease-associated p.Arg329His mutation in AARS1 severely reduces aminoacylation (tRNA charging) enzyme activity, as demonstrated by aminoacylation assays and yeast viability complementation assays. In vitro aminoacylation assay, yeast complementation assay Human mutation High 22009580
2009 AlaRS (AARS1) has an inherent structural dilemma in amino acid recognition: an acidic residue required to pin down the alpha-amino group of alanine serendipitously interacts with the serine OH, explaining why serine is misactivated. Nine crystal structures and kinetic/mutational analysis provided the mechanistic basis. X-ray crystallography (9 structures), kinetic assays, site-directed mutagenesis Nature High 20010690
2021 AARS1 variants causing trichothiodystrophy result in instability of the alanyl-tRNA synthetase protein and a reduced rate of tRNA charging (aminoacylation), as demonstrated by functional studies in patient-derived skin fibroblasts. tRNA charging activity assay in patient fibroblasts, protein stability assessment Human molecular genetics Medium 33909043
2021 CMT2N-associated mutations in the aminoacylation domain of AlaRS (including R329H) induce structural loosening of the aminoacylation domain, enabling aberrant gain-of-function binding to neuropilin 1 (Nrp1); this interaction was confirmed in patient samples and the b1b2 domains of Nrp1 are responsible. Notably, R329H is aminoacylation-normal as a purified protein in vitro. X-ray crystallography, small-angle X-ray scattering, hydrogen-deuterium exchange (HDX), switchSENSE hydrodynamic diameter, protease digestion, Co-immunoprecipitation in patient cells Proceedings of the National Academy of Sciences of the United States of America High 33753480
2016 Crystal structures of human C-Ala (the C-terminal domain of AlaRS) revealed that sequence divergence from prokaryotic C-Ala reshaped the domain architecture, forming a dimer interface with a DNA-binding groove; direct DNA binding by human C-Ala (but not bacterial C-Ala) was demonstrated, indicating a repurposing of this domain in higher organisms. X-ray crystallography (two crystal forms of human C-Ala), small-angle X-ray scattering, in vitro DNA binding assay Proceedings of the National Academy of Sciences of the United States of America High 27911835
2017 D-aminoacyl-tRNA deacylase (DTD) edits mischarged Gly-tRNAAla species (generated by AARS1 mischarging) four orders of magnitude more efficiently than AARS1's own editing activity; DTD knockout in an AlaRS editing-defective background causes pronounced toxicity in E. coli, establishing DTD as a secondary cellular checkpoint for glycine mischarging by AlaRS. In vitro editing/deacylation kinetic assays, genetic epistasis (DTD knockout in AlaRS editing-defective background), in vivo toxicity rescue by alanine supplementation eLife High 28362257
2018 CMT2N-associated AARS1 mutations include both loss-of-function (hypomorphic: p.Ser627Leu, p.Arg326Trp) and gain-of-function (hypermorphic: p.Glu337Lys) alleles; yeast complementation demonstrated the functional class of each, and aminoacylation assays confirmed p.Glu337Lys increases tRNA charging velocity. All three caused neural abnormalities in zebrafish. Yeast complementation assay, in vitro aminoacylation assay, zebrafish expression model Human molecular genetics High 30124830
2018 The CMT2N-associated N71Y mutation of AARS1 causes mislocalization of the protein to lysosomes (instead of cytoplasm) in COS-7 cells, and expression of this mutant in N1E-115 neuronal cells inhibits neurite process growth; this inhibition is reversed by pretreatment with valproic acid. Immunofluorescence localization, neuronal process growth assay, pharmacological rescue Neuroscience research Medium 30261202
2015 A novel AARS1 p.Gly102Arg mutation fails to complement yeast lacking AARS function, demonstrating the mutation is damaging to tRNA synthetase activity; affected individuals present with myeloneuropathy. Yeast complementation assay Neurology Medium 25904691
2020 AARS1 deficiency variants (p.Leu298Gln; p.Arg751Gly) cause decreased aminoacylation (tRNA charging) enzymatic activity in patient-derived fibroblasts, associated with recurrent acute liver failure. Enzymatic activity assay in patient fibroblasts Molecular genetics and metabolism reports Medium 33294374
2025 AARS1 lactylates BLM helicase at Lys24, improving BLM protein stability by inhibiting MIB1-mediated ubiquitination and increasing its interaction with DNA repair factors, thereby promoting DNA end resection and homologous recombination repair, which drives chemoresistance to anthracyclines. Co-immunoprecipitation, mass spectrometry, global lactylome profiling, Lys24 mutation (delactylation), ubiquitination assay Signal transduction and targeted therapy Medium 40634292
2025 AARS1 lactylates histone H3K18 and STAT1, and interacts with STAT1 to jointly regulate ELOVL5 transcription, inducing lipid peroxidation and ferroptosis in diabetic nephropathy; β-alanine inhibits AARS1-mediated lactylation and attenuates ferroptosis in model mice. Co-immunoprecipitation, transcriptomic and lipidomic analyses, AARS1 heterozygous mouse model, molecular biological assays Cell death and differentiation Medium 40987895
2026 AARS1 lactylates STAT1 at K193, inhibiting its binding to JAK2 and phosphorylation, thereby disrupting IFN-γ signaling and reducing downstream chemokine expression (CXCL9/10/11), facilitating tumor immune escape; a cell-penetrating peptide targeting K193 lactylation restored IFN-γ responsiveness. Co-immunoprecipitation, phosphorylation assays, loss-of-function studies, peptide inhibitor Cell reports Medium 41832952
2025 AARS1 directly lactylates Akt and the NF-κB subunit p65, enhancing their phosphorylation and activation, which impairs autophagy, promotes inflammation and tubular injury in diabetic kidney disease; kidney-specific Aars1 knockout or β-alanine treatment reduced these effects in mouse models. CUT and Tag, ChIP assays, luciferase reporter assays, CRISPR/Cas9 KO cells, kidney-specific knockout mice, streptozotocin and db/db diabetic models Cellular & molecular biology letters Medium 42215867
2025 A single-point mutation L219M in AlaRS (from Methylomonas sp.) eliminates serine misactivation; structural analysis revealed that flexibility of Val204 is key to blocking serine binding in the mutant. The same mutation also eliminates the enzyme's inherent lactyltransferase activity, linking the lactate-binding/activation pocket to the serine misactivation mechanism. X-ray crystallography (pre-activation state structure), in vitro aminoacylation kinetic assays, in vitro lactyltransferase assay, site-directed mutagenesis Nucleic acids research Medium 40479712
2026 AARS1 catalyzes lactylation of ATRIP at K127 in neuronal processes during sepsis, triggering ATRIP-ATR complex formation and pathway activation independent of DNA damage, causing excessive autophagy, synaptic dysfunction and neuronal process injury; L-alanine competitively inhibits lactate binding to AARS1 and suppresses this signaling. In vivo CLP sepsis mouse model, AARS1 knockdown, ATR inhibitor, lactylation site mapping, behavioral assays Brain, behavior, and immunity Medium 41713664
2025 AARS1 lactylates Osterix (Osx) transcription factor, increasing its binding to target gene promoters and promoting interaction with WDR5, which facilitates H3K4 tri-methylation on downstream target genes, enhancing osteoblast differentiation; silencing of AARS1 impaired alkaline phosphatase activity and mineralized nodule formation. Chromatin immunoprecipitation, Co-immunoprecipitation, loss-of-function knockdown, ALP activity assay, Alizarin Red staining Acta histochemica Medium 40505545
2026 AARS1 mediates lactylation of AKR1B10 at K173, stabilizing AKR1B10 by blocking MIB1-mediated ubiquitin-proteasomal degradation; stabilized AKR1B10 interacts with LDHA, promotes LDHA Y10 phosphorylation and glycolytic lactate production, which drives H3K18 lactylation and transcriptional upregulation of LDHA, forming a self-reinforcing circuit driving lenvatinib resistance in HCC. Co-immunoprecipitation, mass spectrometry, ubiquitination assay, western blot, functional metabolic assays (Seahorse XF) Clinical and translational medicine Medium 41454479
2024 Comprehensive humanized yeast model assessment of AARS1 recessive disease variants showed the majority cause variable loss-of-function effects; K81T AARS1 demonstrated both loss-of-function and dominant-negative effects, indicating certain AARS1 variants can cause both dominant and recessive phenotypes. Humanized yeast complementation assay (side-by-side comparison of all reported recessive missense variants) bioRxivpreprint Medium 38979321
2025 AARS1 promotes endometriosis by lactylating Snail1 to maintain its protein stability, enhancing epithelial-to-mesenchymal transition in endometriotic stromal cells. Co-immunoprecipitation, loss-of-function knockdown, cell proliferation/migration/invasion assays Biology of reproduction Low 40815826

Source papers

Stage 0 corpus · 46 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2024 Alanyl-tRNA synthetase, AARS1, is a lactate sensor and lactyltransferase that lactylates p53 and contributes to tumorigenesis. Cell 435 38653238
2024 AARS1 and AARS2 sense L-lactate to regulate cGAS as global lysine lactyltransferases. Nature 277 39322678
2024 The alanyl-tRNA synthetase AARS1 moonlights as a lactyltransferase to promote YAP signaling in gastric cancer. The Journal of clinical investigation 243 38512451
2011 A recurrent loss-of-function alanyl-tRNA synthetase (AARS) mutation in patients with Charcot-Marie-Tooth disease type 2N (CMT2N). Human mutation 95 22009580
2009 Paradox of mistranslation of serine for alanine caused by AlaRS recognition dilemma. Nature 87 20010690
2021 Protein instability associated with AARS1 and MARS1 mutations causes trichothiodystrophy. Human molecular genetics 41 33909043
2015 A novel AARS mutation in a family with dominant myeloneuropathy. Neurology 36 25904691
2015 Genotype/phenotype correlations in AARS-related neuropathy in a cohort of patients from the United Kingdom and Ireland. Journal of neurology 35 26032230
2017 Role of D-aminoacyl-tRNA deacylase beyond chiral proofreading as a cellular defense against glycine mischarging by AlaRS. eLife 34 28362257
2018 Hypermorphic and hypomorphic AARS alleles in patients with CMT2N expand clinical and molecular heterogeneities. Human molecular genetics 32 30124830
2025 Irinotecan alleviates chemoresistance to anthracyclines through the inhibition of AARS1-mediated BLM lactylation and homologous recombination repair. Signal transduction and targeted therapy 27 40634292
2021 CMT2N-causing aminoacylation domain mutants enable Nrp1 interaction with AlaRS. Proceedings of the National Academy of Sciences of the United States of America 26 33753480
2019 An AARS variant as the likely cause of Swedish type hereditary diffuse leukoencephalopathy with spheroids. Acta neuropathologica communications 25 31775912
2016 Two crystal structures reveal design for repurposing the C-Ala domain of human AlaRS. Proceedings of the National Academy of Sciences of the United States of America 23 27911835
2020 Alanyl-tRNA synthetase 1 (AARS1) gene mutation in a family with intermediate Charcot-Marie-Tooth neuropathy. Genes & genomics 20 32314272
2021 Expanded phenotype of AARS1-related white matter disease. Genetics in medicine : official journal of the American College of Medical Genetics 19 34446925
2024 AARS Online: A collaborative database on the structure, function, and evolution of the aminoacyl-tRNA synthetases. IUBMB life 16 39247978
2025 AARS1-mediated lactylation of H3K18 and STAT1 promotes ferroptosis in diabetic nephropathy. Cell death and differentiation 13 40987895
2020 Recurrent acute liver failure in alanyl-tRNA synthetase-1 (AARS1) deficiency. Molecular genetics and metabolism reports 12 33294374
2018 CMT type 2N disease-associated AARS mutant inhibits neurite growth that can be reversed by valproic acid. Neuroscience research 11 30261202
2020 The uniqueness of AlaRS and its human disease connections. RNA biology 9 33317386
2025 AARS1 and AARS2: From Protein Synthesis to Lactylation-Driven Oncogenesis. Biomolecules 6 41008630
2022 Gain of C-Ala enables AlaRS to target the L-shaped tRNAAla. Nucleic acids research 6 35100402
2022 Aminoacyl-tRNA synthetase (AARS) as an attractive drug target in neglected tropical trypanosomatid diseases-Leishmaniasis, Human African Trypanosomiasis and Chagas disease. Molecular and biochemical parasitology 6 35988745
2020 Mutations in aARS genes revealed by targeted next-generation sequencing in patients with mitochondrial diseases. Molecular biology reports 6 32319008
2023 Report of A Family with Adult-Onset Leukoencephalopathy with Axonal Spheroids and Pigmented Glia (ALSP) Without Mutations in CSF1R, AARS1 or AARS2. Movement disorders clinical practice 5 36825047
2022 Clinical characteristics and proteome modifications in two Charcot-Marie-Tooth families with the AARS1 Arg326Trp mutation. BMC neurology 5 35971119
2026 AARS1-mediated AKR1B10 lactylation stabilizes an aerobic glycolysis-positive feedback loop to drive lenvatinib resistance in hepatocellular carcinoma. Clinical and translational medicine 4 41454479
2025 AARS1-mediated Osterix lactylation promotes its transcriptional activity during osteoblast differentiation. Acta histochemica 3 40505545
2025 Lactate/AARS1/H3K18la/LDHA positive feedback loop triggers ferroptosis, which participates in diabetic nephropathy via the modulation of ACSL4 transcription. Acta biochimica et biophysica Sinica 3 41169201
2019 Data on the effects of Charcot-Marie-Tooth disease type 2N-associated AARS missense mutation (Arg329-to-His) on the cell biological properties. Data in brief 3 31194127
2025 AARS1 promotes endometriosis progression by promoting the lactylation of Snail1†. Biology of reproduction 2 40815826
2025 AARS1/2: dual functions in protein translation and metabolic- immune regulation. Yi chuan = Hereditas 2 40962470
2024 Comprehensive assessment of recessive, pathogenic AARS1 alleles in a humanized yeast model reveals loss-of-function and dominant-negative effects. bioRxiv : the preprint server for biology 2 38979321
2026 Targeting AARS1-dependent lactylation improves neuronal process plasticity and mitigates cognitive deficits in sepsis-associated encephalopathy. Brain, behavior, and immunity 1 41713664
2025 Unlocking the serine mischarging paradox and inhibiting lactyltransferase activity of AlaRS by a single-point mutation. Nucleic acids research 1 40479712
2009 [aaRS--the etiological factor and the attractive target of many disorders]. Postepy biochemii 1 20201350
2026 Recessive AARS1 variants perturb human and mouse development. HGG advances 0 41508610
2026 AARS1-mediated lactylation of STAT1 drives immune evasion. Cell reports 0 41832952
2026 Comprehensive pan-cancer analysis of AARS1, a newly identified lactyltransferase in human cancers. Cancer cell international 0 41952148
2026 AARS1 promotes diabetic kidney disease through rewiring Akt and NF-κB signaling to suppress autophagy and sustain inflammation. Cellular & molecular biology letters 0 42215867
2025 Circ-AARS plays an important role during the odontogenic differentiation of dental pulp stem cells by modulating miR-24-3p/KLF6 expression. Stem cell research & therapy 0 40083007
2025 Liver Dysfunction and Liver Histopathology in Alanyl-tRNA Synthetase 1 (AARS1) Deficiency with a Novel Mutation: A Case Report. Fetal and pediatric pathology 0 40674726
2024 AARS and CACNA1A mutations: diagnostic insights into a case report of uncommon epileptic encephalopathy phenotypes in two siblings. Frontiers in neurology 0 38689878
2023 High frequency of endoluminal thrombus in patients with ischaemic stroke following AARS-CoV-2 infection. Neurologia 0 38065431
2008 Structural determinants characteristic to AARS subclasses and tRNA-splicing endonuclease in eukaryotes. Journal of biomolecular structure & dynamics 0 18597544

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