Affinage

ASL

Argininosuccinate lyase · UniProt P04424

Length
464 aa
Mass
51.7 kDa
Annotated
2026-06-09
68 papers in source corpus 15 papers cited in narrative 16 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

Argininosuccinate lyase (ASL) is a homotetrameric urea-cycle enzyme whose lyase activity cleaves argininosuccinate to arginine and fumarate, and which serves a broader role in supplying arginine for nitric oxide (NO) production through the citrulline-NO cycle (PMID:30158522, PMID:34861885). Beyond hepatic ammonia detoxification, neuronal ASL is required for brain NO homeostasis: loss of ASL produces nitrosative/oxidative stress independent of hyperammonemia, and combined hepatic plus cerebral correction normalizes NO signaling and rescues neuronal cell death and behavior (PMID:30158522). Through this NO-generating function ASL governs catecholamine biosynthesis in specific brainstem nuclei—it controls tyrosine hydroxylase abundance and activity in locus coeruleus neurons and, in substantia nigra dopaminergic neurons, restrains tyrosine aggregation and α-synuclein elevation, with NO donors rescuing the catecholamine and motor phenotypes in conditional knockouts (PMID:31747589, PMID:34417872). In cancer, ASL acts as an enzymatic-activity-dependent tumor suppressor in clear cell renal cell carcinoma, where it conserves cellular aspartate away from pyrimidine synthesis and modulates NO levels; catalytically dead mutants fail to suppress growth, establishing that lyase catalysis rather than a scaffolding role is responsible (PMID:34861885). ASL expression is itself transcriptionally tuned by upstream regulators, including KLF7 in glioma and a taurine-responsive FOS-ASL axis in hepatocellular carcinoma, linking ASL activity to polyamine biosynthesis and urea-cycle-driven proliferation in tumor contexts (PMID:31018905, PMID:41708583). Loss-of-function mutations cause ASL deficiency: the gene comprises 16 coding exons with mutational hotspots and a predominant splicing variant, and pathogenic missense and splice mutations reduce or abolish enzymatic activity, frequently by disrupting homotetramer assembly (PMID:12384776, PMID:31183366, PMID:26843370).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2002 Medium

    Establishing the genomic architecture of ASL was needed to interpret disease alleles systematically; defining all 16 coding exons and recurrent mutations provided the framework for ASL deficiency genetics.

    Evidence Genomic DNA sequencing and mutation screening across 27 patients

    PMID:12384776

    Open questions at the time
    • Gene structure alone does not establish functional consequence of individual variants
    • No enzymatic or structural readout for the catalogued mutations
  2. 2004 High

    To define which residues are catalytically essential, kinetic dissection of point mutations showed specific positions are required for substrate turnover and protein stability.

    Evidence Site-directed mutagenesis, recombinant enzyme kinetics, thermal stability and CD spectroscopy

    PMID:15471876

    Open questions at the time
    • Performed on a lyase-family context (adenylosuccinate lyase residues) rather than full human urea-cycle catalysis
    • Does not address tetramer-level interactions in the cellular setting
  3. 2007 Medium

    To distinguish coding from splicing pathogenicity and predict missense impact, functional minigene assays plus structural mapping connected variants to tetramer disruption.

    Evidence Hybrid minigene splicing assay and molecular modeling on the ASL crystal structure

    PMID:17326097

    Open questions at the time
    • Structural modeling is computational, not experimentally validated for tetramer disruption
    • Single assay per variant class
  4. 2013 Low

    Extending the structural rationale, mutation mapping argued that pathogenic missense variants disrupt homotetramer formation, offering a unifying structural mechanism for deficiency.

    Evidence Structural mapping onto the published ASL homotetramer

    PMID:24166829

    Open questions at the time
    • Computational only; no experimental validation of tetramer disruption in this study
    • Does not quantify residual enzymatic activity
  5. 2016 Medium

    To determine whether ASL deficiency could be chemically corrected, cysteamine was shown to chemically convert cysteine-substituted residues toward a lysine analogue and partially restore activity, providing a mechanistic rationale for pharmacochaperone-style rescue.

    Evidence Expression of cysteine-for-arginine ASL mutants in 293T cells with cysteamine treatment and activity assays

    PMID:26745957

    Open questions at the time
    • Single lab, cell-based activity readout
    • Applies only to specific arginine-to-cysteine substitutions
  6. 2016 Medium

    To explain why a coding missense variant behaves as a loss-of-function allele, an exon-trapping assay revealed that c.434A>G causes exon 5 skipping, demonstrating a splicing mechanism beyond simple amino-acid change.

    Evidence Exon trapping minigene splicing assay following NGS

    PMID:26843370

    Open questions at the time
    • Single method, single variant
    • No protein-level or enzymatic quantification of the resulting transcript
  7. 2018 High

    Whether ASL has a brain-intrinsic role beyond hepatic ammonia clearance was unresolved; combined hepatic and cerebral gene correction established that neuronal ASL activity is required for NO homeostasis and prevents nitrosative-stress-driven neuronal death independent of hyperammonemia.

    Evidence AAV8 gene transfer in ASL-deficient mice with behavioral, biochemical, and histological readouts

    PMID:30158522

    Open questions at the time
    • Does not map which neuronal populations require ASL most acutely
    • NO source apportionment between cell types not resolved
  8. 2019 High

    To define a specific neuronal output of ASL-dependent NO, locus-coeruleus-specific knockout placed ASL upstream of NO-mediated regulation of tyrosine hydroxylase and catecholamine synthesis, with NO donors rescuing the phenotype.

    Evidence LC-specific conditional knockout mouse, TH activity/abundance measurements, catecholamine quantification, NO donor rescue, seizure/stress phenotyping

    PMID:31747589

    Open questions at the time
    • Molecular link between NO and TH abundance not fully defined
    • Generalization to other catecholaminergic nuclei addressed only later
  9. 2019 Medium

    To determine whether ASL contributes to tumor biology and how, work showed KLF7 transcriptionally activates ASL in glioma and that ASL enhances polyamine biosynthesis to drive proliferation and migration.

    Evidence Transcriptional activation assays and knockdown/overexpression in glioma cells with polyamine metabolite measurement

    PMID:31018905

    Open questions at the time
    • Depth of ChIP/reporter evidence for direct KLF7 binding limited
    • Single lab
  10. 2019 Medium

    Additional patient variants were functionally tested to confirm pathogenicity, showing p.Lys69Arg reduces and p.Arg213* abolishes enzymatic activity in a cellular system.

    Evidence Expression in HEK293T cells with spectrophotometric coupled enzyme assay measuring urea production

    PMID:31183366

    Open questions at the time
    • Single method, single lab
    • No structural correlate for the activity loss
  11. 2019 Low

    Whether reported missense variants act through folding/assembly was addressed by in silico tetramer analysis predicting that four novel variants destabilize the tetramer.

    Evidence In silico structural analysis of the ASL tetramer model

    PMID:31709144

    Open questions at the time
    • Computational prediction only, no experimental tetramer or activity validation
    • Variant-specific residual function unquantified
  12. 2021 High

    To extend the catecholaminergic role to dopaminergic neurodegeneration, conditional ASL loss in catecholamine neurons produced tyrosine aggregates, α-synuclein elevation, and motor/cognitive deficits, all rescued by NO supplementation.

    Evidence Conditional knockout mouse, immunofluorescence, catecholamine and α-synuclein measurement, NO donor rescue, behavioral testing

    PMID:34417872

    Open questions at the time
    • Mechanistic link between NO loss and tyrosine aggregation not molecularly resolved
    • Relevance to idiopathic Parkinsonian pathology not established
  13. 2021 High

    To test whether ASL acts as a tumor suppressor through catalysis or scaffolding, re-expression with activity-dead mutants showed enzymatic activity is required for growth suppression in ccRCC, acting via aspartate conservation away from pyrimidine synthesis and NO regulation.

    Evidence Loss- and gain-of-function in ccRCC lines, xenografts, metabolomics, and catalytically inactive mutants

    PMID:34861885

    Open questions at the time
    • Relative contribution of aspartate conservation versus NO not fully partitioned
    • Context-specificity across tumor types not defined
  14. 2023 Medium

    To establish therapeutic sufficiency of restoring ASL, mRNA-LNP delivery produced robust hepatocyte ASL expression and drastically improved survival in an ASL deficiency mouse model.

    Evidence mRNA-LNP formulation, in vitro expression, IV administration in ASLNeo/Neo mice, survival and cytokine profiling

    PMID:37371829

    Open questions at the time
    • Hepatic restoration may not address cerebral NO/catecholamine phenotypes
    • Durability and repeat-dosing tolerability not fully characterized
  15. 2026 Medium

    To identify how metabolic signals tune ASL in cancer, taurine was shown to act through a FOS-ASL transcriptional axis to suppress urea cycle activity and HCC tumor growth.

    Evidence Target identification, FOS-ASL transcription analysis, knockdown/overexpression in HCC lines, metabolic and tumor growth assays

    PMID:41708583

    Open questions at the time
    • Direct physical taurine-ASL interaction not biochemically demonstrated
    • Single mechanistic context (HCC)

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ASL-dependent NO generation is biochemically coupled to tyrosine hydroxylase abundance and tyrosine aggregation, and how its catalytic versus metabolite-channeling roles are partitioned across hepatic, neuronal, and tumor contexts, remain unresolved.
  • No molecular mechanism connecting NO levels to TH protein stability
  • No reconciliation of ASL as urea-cycle enzyme versus NO-cycle effector at the structural level
  • Tumor-context dependence (suppressor in ccRCC, proliferative in glioma/HCC) mechanistically unexplained

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0016787 hydrolase activity 2 GO:0016829 lyase activity 2
Pathway
R-HSA-1430728 Metabolism 4 R-HSA-1643685 Disease 3
Partners
ASS1FOSKLF7
Complex memberships
ASL homotetramer

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2018 ASL (argininosuccinate lyase) participates in the citrulline-nitric oxide (NO) cycle in neurons; ASL deficiency causes neuronal oxidative/nitrosative stress independent of hyperammonemia. Intravenous AAV8 vector delivery correcting both hepatic and cerebral ASL activity normalized NO signaling, reduced cortical cell death, and improved behavior in ASL-deficient mice, establishing that neuronal ASL activity is required for NO homeostasis in the brain. AAV8-mediated gene transfer in ASL-deficient mice, behavioral assays, neuronal cell death quantification, NO pathway biochemistry Nature communications High 30158522
2019 ASL is expressed in neurons of the nucleus locus coeruleus (LC) and metabolically regulates tyrosine hydroxylase (TH) activity and abundance through nitric oxide (NO) signaling. LC-specific ASL conditional knockout mice show reduced TH amount and activity, decreased catecholamine synthesis, altered stress response, and increased seizure reactivity; NO donors rescue catecholamine levels, seizure sensitivity, and stress response, placing ASL upstream of NO-mediated TH regulation. Conditional knockout mouse (LC-ASL-cKO), LC-specific TH activity and protein measurements, catecholamine quantification, NO donor pharmacological rescue, behavioral/seizure phenotyping Cell reports High 31747589
2021 ASL is expressed in dopaminergic neurons of the substantia nigra pars compacta (including ALDH1A1+ subpopulation). Conditional loss of ASL in catecholamine neurons causes catecholamine deficiency, accumulation of tyrosine aggregates, elevation of α-synuclein, and motor/cognitive deficits. NO supplementation rescues aggregate formation and motor deficits, linking ASL-dependent NO production to tyrosine metabolism and neurodegeneration. Conditional knockout mouse model, immunofluorescence, catecholamine and α-synuclein measurements, NO donor rescue, behavioral testing Human genetics High 34417872
2021 ASL (argininosuccinate lyase) enzymatic activity is required for tumor suppression in clear cell renal cell carcinoma (ccRCC). Re-expression of ASL (with ASS1) suppresses growth in 2D, 3D, and xenograft models in an enzymatic-activity-dependent manner. ASL-mediated effects involve conservation of cellular aspartate (redirecting it away from pyrimidine synthesis) and regulation of nitric oxide synthesis. Loss-of-function (KO in HK-2 cells), gain-of-function re-expression in ccRCC lines, xenograft mouse models, metabolomic analysis, enzymatic activity mutants Cancer & metabolism High 34861885
2019 KLF7 transcriptionally activates ASL gene expression in glioma cells, and ASL in turn enhances polyamine biosynthesis (a urea cycle metabolite pathway), contributing to glioma cell proliferation, migration, and tumorigenesis. Transcriptional activation assays (luciferase/ChIP implied by 'transcriptionally activated'), functional knockdown/overexpression in glioma cells, polyamine metabolite measurements Biochemical and biophysical research communications Medium 31018905
2004 Mutations in human adenylosuccinate lyase (ASL; EC 4.3.2.2) at positions E80D and D87E (equivalent to positions 62 and 69 in Bacillus subtilis ASL) reduce enzymatic Vmax for conversion of adenylosuccinate to AMP and fumarate and increase Km for adenylosuccinate; the D87E (position 69) mutation has modest effect while the E80D-equivalent (position 62, D→E change) causes the most drastic reduction in activity and stability, demonstrating the catalytic importance of these residues. Site-directed mutagenesis, recombinant protein expression and purification, enzyme kinetics (Vmax, Km measurements), thermal stability assay, CD spectroscopy The Journal of biological chemistry High 15471876
2016 Cysteamine treatment of cells expressing cysteine-for-arginine ASL mutants (p.Arg94Cys, p.Arg379Cys, p.Arg385Cys) increases ASL enzymatic activity by chemically modifying the substituted cysteine to a lysine analogue, partially restoring function; p.Arg385Cys activity after cysteamine treatment resembles the designed p.Arg385Lys mutant, providing mechanistic evidence for the cysteamine action. Mammalian expression system (293T cells), transfection of ASL cysteine-for-arginine mutants, enzyme activity assay with and without cysteamine treatment Molecular diagnosis & therapy Medium 26745957
2016 A missense mutation c.434A>G (p.D145G) in exon 5 of the ASL gene drives alternative splicing, causing loss of exon 5 in the mRNA, as demonstrated by exon trapping assay. Next generation sequencing, exon trapping (minigene splicing assay) BMC medical genetics Medium 26843370
2007 Pathogenicity of ASL splicing mutations was confirmed by functional splicing assay using a hybrid minigene. Molecular modeling using the reported 3D structure of ASL was used to predict functional consequences of missense mutations on homotetramer formation. Hybrid minigene splicing assay, molecular modeling based on ASL crystal structure, genomic DNA mutation analysis Human mutation Medium 17326097
2013 Structural analysis of ASL mutations demonstrates that pathogenic missense variants disrupt homotetramer formation by altering bonding with neighboring residues, providing a structural mechanism for ASL deficiency. Structural considerations based on published ASL homotetramer structure, mutation mapping Human mutation Low 24166829
2019 Structural examination of four novel pathogenic ASL variants (Leu260Arg, Ser447Thr, Arg146Gly, Leu199Val) revealed that all affect stability of the tetrameric ASL structure by disturbing bonding with neighboring residues. In silico structural analysis of ASL tetramer model Molecular genetics and metabolism reports Low 31709144
2023 ASL-encoding mRNA formulated in lipid nanoparticles (LNP) produces robust ASL protein expression in vitro and in vivo, and intravenous administration in ASLNeo/Neo mice (ASLD model) drastically improves survival, demonstrating that restored ASL enzymatic activity in hepatocytes is sufficient to correct the metabolic deficit. mRNA-LNP formulation, in vitro expression in human cells, IV administration in ASLNeo/Neo mouse model, survival assay, cytokine profiling Biomedicines Medium 37371829
2019 ASL enzymatic activity is required for its tumor-suppressive function in ccRCC; catalytically inactive ASL mutants do not suppress growth, establishing that the lyase catalytic activity (cleaving argininosuccinate to arginine and fumarate) rather than a structural/scaffold role mediates growth suppression. Expression of enzymatic activity mutants in ccRCC cell lines, 2D/3D growth assays, xenograft models Cancer & metabolism High 34861885
2026 Taurine suppresses urea cycle activity by targeting ASL as its main effector in hepatocellular carcinoma (HCC) cells. FOS proto-oncogene functions as a transcription factor for ASL; taurine treatment reduces FOS levels, thereby suppressing ASL expression and urea cycle activity. The FOS-ASL axis is required for the metabolic effects of taurine on HCC tumor growth. Target identification (ASL identified as taurine's main target), transcription factor analysis (FOS-ASL axis), knockdown/overexpression in HCC cell lines, metabolic assays, tumor growth assays Cell death discovery Medium 41708583
2002 The complete ASL gene structure was determined, comprising 16 coding exons, enabling systematic mutation analysis. Mutational hotspots were identified in exons 4, 5, and 7, and a predominant splicing mutation IVS5+1G→A was found on 15 alleles, establishing the genomic architecture of ASL deficiency. Genomic DNA sequencing, PCR-based mutation screening of all 16 coding exons, identification of transcript variants Human genetics Medium 12384776
2019 Novel ASL mutation c.206A>G (p.Lys69Arg) significantly reduces ASL enzymatic activity when expressed in HEK293T cells, while the p.Arg213* nonsense mutation abolishes activity entirely, confirming pathogenicity and establishing the functional importance of these residues. Expression of ASL constructs in HEK293T cells, spectrophotometric coupled enzyme assay measuring urea production BioMed research international Medium 31183366

Source papers

Stage 0 corpus · 68 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2020 Eculizumab treatment in patients with COVID-19: preliminary results from real life ASL Napoli 2 Nord experience. European review for medical and pharmacological sciences 290 32329881
1983 Pharmacology of ASL-8052, a novel beta-adrenergic receptor antagonist with an ultrashort duration of action. Journal of cardiovascular pharmacology 76 6193366
2005 Neural organization for recognition of grammatical and emotional facial expressions in deaf ASL signers and hearing nonsigners. Brain research. Cognitive brain research 65 15653293
1997 Face processing by deaf ASL signers: evidence for expertise in distinguished local features. Journal of deaf studies and deaf education 63 15579849
2017 Glioma Grading and Determination of IDH Mutation Status and ATRX loss by DCE and ASL Perfusion. Clinical neuroradiology 57 28488024
2005 The efficacy of a novel insecticidal protein, Allium sativum leaf lectin (ASAL), against homopteran insects monitored in transgenic tobacco. Plant biotechnology journal 47 17147631
2007 Argininosuccinate lyase deficiency: mutational spectrum in Italian patients and identification of a novel ASL pseudogene. Human mutation 42 17326097
2009 Tissue specific expression of potent insecticidal, Allium sativum leaf agglutinin (ASAL) in important pulse crop, chickpea (Cicer arietinum L.) to resist the phloem feeding Aphis craccivora. Transgenic research 41 19184504
2012 ASL/LBD phylogeny suggests that genetic mechanisms of root initiation downstream of auxin are distinct in lycophytes and euphyllophytes. Molecular biology and evolution 40 23112232
2018 Argininosuccinic aciduria fosters neuronal nitrosative stress reversed by Asl gene transfer. Nature communications 38 30158522
2013 Mutations and polymorphisms in the human argininosuccinate lyase (ASL) gene. Human mutation 37 24166829
2008 Transgenic rice expressing Allium sativum leaf agglutinin (ASAL) exhibits high-level resistance against major sap-sucking pests. BMC plant biology 37 18854007
2019 KLF7 promotes polyamine biosynthesis and glioma development through transcriptionally activating ASL. Biochemical and biophysical research communications 35 31018905
2018 CEST, ASL, and magnetization transfer contrast: How similar pulse sequences detect different phenomena. Magnetic resonance in medicine 33 29845640
2011 Methods for ASL measurements and mucus transport rates in cell cultures. Methods in molecular biology (Clifton, N.J.) 33 21547727
2002 Argininosuccinate lyase (ASL) deficiency: mutation analysis in 27 patients and a completed structure of the human ASL gene. Human genetics 33 12384776
2020 Increased blood-brain barrier permeability to water in the aging brain detected using noninvasive multi-TE ASL MRI. Magnetic resonance in medicine 31 32910547
2021 ASS1 and ASL suppress growth in clear cell renal cell carcinoma via altered nitrogen metabolism. Cancer & metabolism 30 34861885
2019 ASL Metabolically Regulates Tyrosine Hydroxylase in the Nucleus Locus Coeruleus. Cell reports 27 31747589
1991 Cortisol induces rapid accumulation of whey acid protein mRNA but not of asl and b-casein mRNA in rabbit mammary explants. Cell biology international reports 27 2029731
1996 Competition on the face: affect and language in ASL motherese. Journal of child language 25 8733568
1983 Cardiovascular pharmacology of ASL-8052, an ultra-short acting beta blocker. European journal of pharmacology 25 6140172
2012 The Neurospora crassa OS MAPK pathway-activated transcription factor ASL-1 contributes to circadian rhythms in pathway responsive clock-controlled genes. Fungal genetics and biology : FG & B 24 22240319
1984 Beta-blocking and hemodynamic effects of ASL-8052. Journal of cardiovascular pharmacology 24 6084788
2013 Synthetic fusion-protein containing domains of Bt Cry1Ac and Allium sativum lectin (ASAL) conferred enhanced insecticidal activity against major lepidopteran pests. Journal of biotechnology 22 24355805
1999 Stress in ASL: empirical evidence and linguistic issues. Language and speech 20 10767990
2018 Multifaceted assessment of the APP/PS1 mouse model for Alzheimer's disease: Applying MRS, DTI, and ASL. Brain research 19 30077647
2004 Two novel mutant human adenylosuccinate lyases (ASLs) associated with autism and characterization of the equivalent mutant Bacillus subtilis ASL. The Journal of biological chemistry 19 15471876
2013 Mapping the hemodynamic response in human subjects to a dopaminergic challenge with dextroamphetamine using ASL-based pharmacological MRI. NeuroImage 18 23296186
2013 Development of transgenic cotton lines expressing Allium sativum agglutinin (ASAL) for enhanced resistance against major sap-sucking pests. PloS one 18 24023750
2011 Pyramiding of Ryd2 and Ryd3 conferring tolerance to a German isolate of Barley yellow dwarf virus-PAV (BYDV-PAV-ASL-1) leads to quantitative resistance against this isolate. TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik 18 21416402
2011 Molecular modeling of Bt Cry1Ac (DI-DII)-ASAL (Allium sativum lectin)-fusion protein and its interaction with aminopeptidase N (APN) receptor of Manduca sexta. Journal of molecular graphics & modelling 18 22182469
2021 ASL expression in ALDH1A1+ neurons in the substantia nigra metabolically contributes to neurodegenerative phenotype. Human genetics 17 34417872
2019 Thermostability enhancement of the α-carbonic anhydrase from Sulfurihydrogenibium yellowstonense by using the anchoring-and-self-labelling-protein-tag system (ASLtag). Journal of enzyme inhibition and medicinal chemistry 17 31039618
2016 Glial fibrillary acidic protein (GFAP) immunoreactivity correlates with cortical perfusion parameters determined by bolus tracking arterial spin labelling (bt-ASL) magnetic resonance (MR) imaging in the Wistar Kyoto rat. Physiology & behavior 17 27068181
2011 Pyramided rice lines harbouring Allium sativum (asal) and Galanthus nivalis (gna) lectin genes impart enhanced resistance against major sap-sucking pests. Journal of biotechnology 17 21295625
2022 The SLC26A9 inhibitor S9-A13 provides no evidence for a role of SLC26A9 in airway chloride secretion but suggests a contribution to regulation of ASL pH and gastric proton secretion. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 14 36183361
2018 Expression of hybrid fusion protein (Cry1Ac::ASAL) in transgenic rice plants imparts resistance against multiple insect pests. Scientific reports 14 29855556
1998 Determination of p185 and adenylosuccinate lyase (ASL) activity in preneoplastic colon lesions and intestinal mucosa of human subjects. Clinical biochemistry 11 9812171
1976 The effect of specific antiserum on the metabolism of three membrane-associated antigens of ASL-1 x LM(TK)- hybrid cells. Somatic cell genetics 10 1027145
2023 ASL mRNA-LNP Therapeutic for the Treatment of Argininosuccinic Aciduria Enables Survival Benefit in a Mouse Model. Biomedicines 8 37371829
2014 Comparing segmented ASL perfusion of vascular territories using manual versus semiautomated techniques in children with sickle cell anemia. Journal of magnetic resonance imaging : JMRI 8 24920128
1982 Cardiovascular pharmacology of ASL-7022, a novel catecholamine. I. Inotropic, chronotropic and pressor actions. The Journal of pharmacology and experimental therapeutics 8 7120130
2023 Molecular-enriched functional connectivity in the human brain using multiband multi-echo simultaneous ASL/BOLD fMRI. Scientific reports 7 37474568
2019 Pancreatic perfusion modulation following glucose stimulation assessed by noninvasive arterial spin labeling (ASL) MRI. Journal of magnetic resonance imaging : JMRI 6 31410924
2016 NGS in argininosuccinic aciduria detects a mutation (D145G) which drives alternative splicing of ASL: a case report study. BMC medical genetics 6 26843370
2023 Utilizing Reduced Labeled Proton Clearance to Identify Preclinical Alzheimer Disease with 3D ASL MRI. Case reports in neurology 5 37901133
2016 Effect of Cysteamine on Mutant ASL Proteins with Cysteine for Arginine Substitutions. Molecular diagnosis & therapy 5 26745957
2024 Alterations in hippocampal somatostatin interneurons, GABAergic metabolism, and ASL perfusion in an aged male mouse model of POCD aggravated by sleep fragmentation. Physiological reports 4 39648073
2019 Chemical Synthesis of Oligoribonucleotide (ASL of tRNALys T. brucei) Containing a Recently Discovered Cyclic Form of 2-Methylthio-N6 -threonylcarbamoyladenosine (ms2 ct6 A). Chemistry (Weinheim an der Bergstrasse, Germany) 4 31328310
2014 [Genetic analysis of ASS1, ASL and SLC25A13 in citrullinemia patients]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 4 24927999
2023 Application study of DTI combined with ASL in the crossed cerebellar diaschisis after subacute cerebral hemorrhage. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 3 37335404
2019 Identification of mutations in Malaysian patients with argininosuccinate lyase (ASL) deficiency. Molecular genetics and metabolism reports 3 31709144
2017 [Mutational analysis of ASS1, ASL and SLC25A13 genes in six Chinese patients with citrullinemia]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 3 28981931
2024 Identification of Novel and Recurrent Variants in BTD, GBE1, AGL and ASL Genes in Families with Metabolic Disorders in Saudi Arabia. Journal of clinical medicine 2 38592052
2023 ThrRS-Mediated Translation Regulation of the RNA Polymerase III Subunit RPC10 Occurs through an Element with Similarity to Cognate tRNA ASL and Affects tRNA Levels. Genes 2 36833389
1979 Inhibition of growth of ASL-1w murine leukemia cells by anti-thymus leukemia antigen (TL) serum in the absence of complement. Journal of immunology (Baltimore, Md. : 1950) 2 489968
2026 Similarity of Biological Information Captured by [68]Ga-PSMA-11 PET and ASL Perfusion MRI in Glioblastoma. AJNR. American journal of neuroradiology 1 40841161
2014 Paget's disease population analysis within Rheumatology Outpatient of the ASL of Biella (Piedmont Region, Italy). Clinical cases in mineral and bone metabolism : the official journal of the Italian Society of Osteoporosis, Mineral Metabolism, and Skeletal Diseases 1 25002880
2008 [Managing waiting lists outpatients clinic. An experience in ASL 4--Turin]. Annali di igiene : medicina preventiva e di comunita 1 18590049
2000 [Rare cause of tachy-, asl well asl bradycardic arrhythmias]. Zeitschrift fur Kardiologie 1 11149266
2026 [Hospital-territory integration: the case of the Territorial Oncology Center of the ASL 04 of Teramo]. Recenti progressi in medicina 0 41568633
2026 Taurine is a natural suppressor of urea cycle via targeting ASL. Cell death discovery 0 41708583
2025 Looking at Viewpoint in ASL Through a Cognitive Linguistics Lens. Wiley interdisciplinary reviews. Cognitive science 0 40107877
2025 [Telemonitoring in heart failure: methodology and results of ASL Nuoro's 2-year experience]. Giornale italiano di cardiologia (2006) 0 40864487
2025 Screening of targets related to amino acid metabolism in glioma to identify the tumor-promoting effects of its core gene ASL. Scientific reports 0 41174115
2023 Research on Wind Turbine Fault Detection Based on the Fusion of ASL-CatBoost and TtRSA. Sensors (Basel, Switzerland) 0 37571525
2019 Whole-Exome Sequencing Identified a Novel Compound Heterozygous Genotype in ASL in a Chinese Han Patient with Argininosuccinate Lyase Deficiency. BioMed research international 0 31183366

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