Affinage

ASPH

Aspartyl/asparaginyl beta-hydroxylase · UniProt Q12797

Length
758 aa
Mass
85.9 kDa
Annotated
2026-06-09
70 papers in source corpus 14 papers cited in narrative 14 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

ASPH is the catalytic aspartyl/asparaginyl β-hydroxylase encoded together with the calsequestrin-binding isoform junctin and the noncatalytic isoform humbug from a single ~200 kb locus that uses separate promoters and alternative splicing (PMID:10956665). As a 2-oxoglutarate-dependent dioxygenase, ASPH performs stereoselective (3R)-hydroxylation of aspartyl/asparaginyl residues through dioxygen activation, hydrogen-atom transfer, and a rate-limiting rebound step, employing an atypical Fe(II) coordination in which a water molecule stabilized by the second-sphere residue Asp721 substitutes for the usual His-His-Asp/Glu triad, with the TPR domain shaping substrate binding (PMID:38455014). This catalytic activity, not mere expression, drives cancer cell migration, EMT, and metastasis, as a hydroxylase-dead mutant fails to promote migration and ASPH physically engages the EMT regulator vimentin (PMID:29764768). Mechanistically, ASPH operates as a hub for oncogenic signaling: it interacts with Notch receptors, JAG ligands, and ADAM10/17 to activate Notch and license pro-metastatic exosome release (PMID:31694640), cooperates with INPP5F to amplify Notch-driven c-MYC/cyclin E1 expression and proliferation (PMID:34996491), and partners with RUVBL2 to enhance MAPK and Notch signaling in lung adenocarcinoma (PMID:41454078). ASPH additionally upregulates SQSTM1/p62 and the SLC7A11-GPX4 axis to promote autophagy while suppressing ferroptosis, and its loss sensitizes hepatocellular carcinoma to sorafenib (PMID:39706251), and it regulates osteogenic differentiation and senescence of mesenchymal stem cells through GSK3β/Wnt signaling (PMID:33015050). Genetically, homozygous loss-of-function mutations that impair hydroxylase activity cause Traboulsi syndrome (facial dysmorphism, lens dislocation, anterior-segment abnormalities), recapitulated by Asph-knockout mice (PMID:24768550), while rare heterozygous variants acting through the junctin isoform cause exertional heat illness and malignant hyperthermia susceptibility (PMID:35697689).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2000 High

    Established that one genomic locus produces three functionally distinct products—the catalytic hydroxylase ASPH, the calsequestrin-binding junctin, and the noncatalytic humbug—resolving how a single gene contributes to both enzymatic and structural roles.

    Evidence Gene cloning, Northern/Western blot, monoclonal antibody epitope mapping, and genomic characterization in mouse

    PMID:10956665

    Open questions at the time
    • Tissue-specific regulation of the three promoters not defined
    • Physiological substrates of the catalytic isoform not identified at this stage
  2. 2014 High

    Demonstrated that loss of ASPH hydroxylase function causes a defined human developmental disorder, linking the enzyme to anterior-segment and craniofacial development.

    Evidence Autozygosity mapping, whole-exome sequencing, and an Asph-knockout mouse with foreshortened-snout phenotype

    PMID:24768550

    Open questions at the time
    • Direct hydroxylation substrates responsible for the lens/zonule phenotype not biochemically validated
    • Mechanism connecting hydroxylase loss to ectopia lentis unresolved
  3. 2018 Medium

    Distinguished catalytic activity from expression as the driver of metastatic behavior, showing the enzyme's hydroxylase function is required for migration and EMT.

    Evidence Wild-type vs. hydroxylase-dead mutant overexpression with migration/metastasis assays and co-IP with vimentin in HCC

    PMID:29764768

    Open questions at the time
    • Whether vimentin is a direct hydroxylation substrate unproven
    • Single-lab co-IP without reciprocal structural mapping
  4. 2019 Medium

    Defined ASPH as an upstream activator of Notch signaling via physical engagement of receptors, JAG ligands, and ADAM10/17, linking it to a druggable pro-metastatic exosome program.

    Evidence Co-IP, CRISPR-KO and overexpression lines, luciferase reporter, invasion assays, and orthotopic/tail-vein mouse models with small-molecule inhibitors

    PMID:31694640

    Open questions at the time
    • Direct hydroxylation of Notch-pathway substrates not demonstrated
    • Single lab; SMI specificity not orthogonally confirmed
  5. 2019 Low

    Proposed FBN1 and LTBP2 as ASPH substrates linking hydroxylation to microfibril and ciliary zonule formation, offering a molecular hypothesis for the lens phenotype.

    Evidence Exome sequencing of a proband plus bioinformatic hydroxylation-motif search in SwissProt

    PMID:30600741

    Open questions at the time
    • Computational prediction without in vitro hydroxylation validation
    • No demonstration that ASPH hydroxylates FBN1/LTBP2 in cells
  6. 2020 Medium

    Extended ASPH function to stem-cell biology, showing it controls osteogenic differentiation and senescence through GSK3β/Wnt signaling.

    Evidence Asph depletion and overexpression in BMSCs with differentiation assays and GSK3β/Wnt Western blots

    PMID:33015050

    Open questions at the time
    • Direct molecular link between ASPH and GSK3β not established
    • Whether the effect requires hydroxylase activity untested
  7. 2022 Medium

    Identified INPP5F as a partner that requires cytoplasmic translocation to drive ASPH-mediated Notch activation and proliferation, adding a regulatory layer to ASPH-Notch signaling.

    Evidence Reciprocal co-IP, mass spectrometry, immunofluorescence, NLS/NES mutagenesis, and LMB treatment in HCC

    PMID:34996491

    Open questions at the time
    • How INPP5F mechanistically potentiates ASPH catalysis unknown
    • Single-lab interaction data
  8. 2022 High

    Established that heterozygous ASPH variants acting through the junctin isoform cause exertional heat illness and malignant hyperthermia susceptibility, demonstrating a distinct excitation-contraction-coupling disease mechanism.

    Evidence Genomic sequencing with validation in CRISPR-edited C2C12 myotubes and transgenic zebrafish

    PMID:35697689

    Open questions at the time
    • Precise effect of variants on junctin-calsequestrin/RyR coupling not fully resolved
    • Relationship to the catalytic isoform's functions not addressed
  9. 2023 Low

    Linked ASPH to a GSK3β/SHH/GLI2 axis driving EMT and metastasis in cholangiocarcinoma, broadening its oncogenic signaling reach.

    Evidence Western blot, wound-healing/transwell assays, and a nude-mouse lung metastasis model

    PMID:37132101

    Open questions at the time
    • Correlative Western-blot analysis without direct ASPH-GSK3β interaction validation
    • Causality of the SHH/GLI2 axis not mechanistically dissected
  10. 2024 Medium

    Resolved the atypical catalytic mechanism, showing ASPH uses a water-mediated Fe(II) coordination via second-sphere Asp721 in place of the canonical triad, with rebound hydroxylation rate-limiting.

    Evidence MD and QM/MM modeling built on published crystal structures

    PMID:38455014

    Open questions at the time
    • Computational model not confirmed by enzyme kinetics or mutagenesis here
    • TPR-domain dynamics during substrate turnover not experimentally validated
  11. 2024 Medium

    Connected ASPH to redox and survival control, showing it promotes autophagy and suppresses ferroptosis via SQSTM1/p62 and SLC7A11-GPX4, with loss sensitizing tumors to sorafenib.

    Evidence ASPH knockout with Western blot, viability assays, and intrahepatic/pulmonary/splenic metastasis mouse models

    PMID:39706251

    Open questions at the time
    • Whether the autophagy/ferroptosis effects depend on hydroxylase activity untested
    • Direct substrate within the SLC7A11-GPX4 axis not identified
  12. 2024 Low

    Modeled how clinical second-sphere and long-range mutations perturb 2OG/substrate binding and HAT activation energies, offering a structural rationale for disease-linked variants.

    Evidence QM/MM and MD computational analysis of mutant vs. wild-type AspH

    PMID:38839574

    Open questions at the time
    • No in vitro biochemical validation of altered activity
    • Clinical genotype-phenotype correlations not experimentally tested
  13. 2025 Medium

    Identified RUVBL2 and HRASLS2 as new ASPH partners, the former amplifying MAPK/Notch signaling and the latter stabilizing ASPH protein, expanding the regulatory network around ASPH in lung and pancreatic cancers.

    Evidence IP-MS and co-IP with epistasis rescue, metabolic/glycolysis assays, and murine metastasis/xenograft models

    PMID:40833600 PMID:41454078

    Open questions at the time
    • Mechanism by which RUVBL2 enhances signaling not defined
    • How HRASLS2 stabilizes ASPH (e.g., ubiquitination) not resolved
    • Single-lab interaction data each

Open questions

Synthesis pass · forward-looking unresolved questions
  • The direct physiological hydroxylation substrates that link ASPH catalysis to its developmental phenotypes and oncogenic signaling outputs remain experimentally unconfirmed.
  • No validated endogenous substrate ties hydroxylase activity to Notch, EMT, or zonule defects
  • Whether protein-interaction effects require catalytic activity largely untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016491 oxidoreductase activity 2 GO:0140096 catalytic activity, acting on a protein 2 GO:0016787 hydrolase activity 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1266738 Developmental Biology 2 R-HSA-1643685 Disease 2
Partners
ADAM10ADAM17HRASLS2INPP5FJAG1NOTCHRUVBL2VIM

Evidence

Reading pass · 14 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 The mouse ASPH (BAH) gene encodes aspartyl β-hydroxylase, a catalytic enzyme, and shares exons with junctin (a calsequestrin-binding protein) and a noncatalytic isoform called humbug (lacking the catalytic domain); all three genes use separate promoters and alternative splicing from the same genomic locus of ~200 kb with 24 exons. Gene cloning, Northern blot, Western blot, monoclonal antibody epitope mapping, genomic characterization The Journal of biological chemistry High 10956665
2014 Homozygous loss-of-function mutations in ASPH (truncating and missense) cause Traboulsi syndrome (facial dysmorphism, lens dislocation, anterior-segment abnormalities, spontaneous filtering blebs); the mutations are predicted to severely impair the enzymatic hydroxylase function of ASPH, and Asph-knockout mice show foreshortened snout phenotype consistent with the human syndrome. Autozygosity mapping, whole-exome sequencing, Sanger sequencing, Asph-knockout mouse model, developmental expression analysis American journal of human genetics High 24768550
2018 The hydroxylase catalytic activity of ASPH (not merely its expression) is required for promoting hepatocellular carcinoma (HCC) cell migration and EMT in vitro and intrahepatic/distant metastasis in vivo; a hydroxylase-dead ASPH mutant fails to promote migration. ASPH physically interacts with vimentin, an EMT regulator, and this interaction mediates its pro-migratory effect. Wild-type vs. hydroxylase mutant overexpression, cell migration assay, in vivo metastasis model, co-immunoprecipitation with vimentin EBioMedicine Medium 29764768
2019 ASPH physically interacts with Notch receptors, Notch ligands (JAGs), and Notch regulators (ADAM10/17) to activate the Notch signaling cascade; this activation provides substrates (especially MMPs/ADAMs) for synthesis and release of pro-metastatic exosomes. Small molecule inhibitors (SMIs) of ASPH's β-hydroxylase activity abrogate these effects. Co-immunoprecipitation, Western blot, lentiviral overexpression and CRISPR-KO stable lines, luciferase reporter, 2D/3D invasion assay, orthotopic and tail vein mouse models Molecular cancer Medium 31694640
2022 Rare heterozygous pathogenic variants in ASPH, which encodes junctin (a regulator of excitation-contraction coupling), cause exertional heat illness and malignant hyperthermia susceptibility; pathogenicity was validated in CRISPR-edited C2C12 myotubes and transgenic zebrafish. Genomic sequencing, CRISPR-edited C2C12 myotubes, transgenic zebrafish models Nature communications High 35697689
2019 Bioinformatic analysis identified 105 putative ASPH hydroxylation substrates in the human proteome; among these, fibrillin-1 (FBN1) and LTBP2—both associated with inherited ectopia lentis—contain the ASPH hydroxylation motif and are essential for microfibril and ciliary zonule development, implicating ASPH-mediated hydroxylation in zonule formation and lens stability. Exome sequencing of proband, bioinformatic motif search in SwissProt database Ophthalmic genetics Low 30600741
2024 AspH (ASPH) catalyzes stereoselective (3R)-hydroxylation of aspartyl- and asparaginyl-residues via a dioxygen activation–HAT–rebound hydroxylation mechanism. Unusually for 2OG hydroxylases, AspH lacks the standard Asp/Glu of the His-His-Asp/Glu Fe-binding triad; instead, a water molecule stabilized by second-coordination-sphere residue Asp721 coordinates Fe(II). The rebound hydroxylation step (not HAT) is rate-limiting. The TPR domain influences substrate binding and undergoes dynamic motions during catalysis. Molecular dynamics (MD), quantum mechanics/molecular mechanics (QM/MM), analysis of published crystal structures Chemical science Medium 38455014
2024 Clinical mutations in second-coordination-sphere (R735W, R735Q, R688Q) and long-range (G434V) residues of AspH alter binding interactions with co-substrate 2-oxoglutarate and substrate in ferryl complexes, and change activation energies for the HAT step, compared to wild-type. These mutations are linked to Traboulsi syndrome and chronic kidney disease. QM/MM and MD computational analysis of mutant vs. wild-type AspH Chemphyschem Low 38839574
2022 INPP5F interacts physically with ASPH (co-immunoprecipitation) and activates the Notch signaling pathway via this interaction to upregulate c-MYC and cyclin E1, promoting HCC cell proliferation; cytoplasmic translocation of INPP5F (regulated by NES/NLS signals) is required for this ASPH-mediated Notch activation. Co-immunoprecipitation, mass spectrometry, immunofluorescence, transcriptome sequencing, nuclear export inhibitor (LMB) treatment, NLS/NES mutagenesis Journal of experimental & clinical cancer research Medium 34996491
2024 ASPH upregulates SQSTM1/P62 and the SLC7A11-GPX4 axis, thereby promoting autophagy but blocking ferroptosis in HCC cells; ASPH knockout sensitizes HCC cells to sorafenib by attenuating autophagy and enabling senescence, apoptosis, and ferroptosis. ASPH promotes tumor growth and metastasis in vivo. ASPH knockout (KO), Western blot, cell viability assay, in vivo HCC mouse models (intrahepatic, pulmonary, splenic metastasis) Cancer letters Medium 39706251
2020 ASPH regulates osteogenic differentiation and cellular senescence of bone marrow mesenchymal stem cells (BMSCs) through Wnt signaling mediated by GSK3β; depletion of Asph suppressed osteogenic differentiation and accelerated senescence, while overexpression had the opposite effect. Asph depletion and overexpression in BMSCs, osteogenic differentiation assay, Western blot for GSK3β/Wnt pathway components Frontiers in cell and developmental biology Medium 33015050
2023 ASPH overexpression promotes epithelial-to-mesenchymal transition (EMT) and metastasis in intrahepatic cholangiocarcinoma cells via a GSK3β/SHH/GLI2 axis: ASPH overexpression decreases phospho-GSK3β and upregulates SHH signaling elements GLI2 and SUFU. Knockdown of ASPH inhibits migration and invasion. Western blot, wound healing assay, transwell assay, immunofluorescence, nude mouse lung metastasis model Current protein & peptide science Low 37132101
2025 ASPH interacts physically with RUVBL2 (identified by immunoprecipitation combined with mass spectrometry) and enhances activation of MAPK and Notch signaling pathways through this interaction to promote lung adenocarcinoma cell migration and metastasis. Immunoprecipitation combined with mass spectrometry (IP-MS), transcriptome sequencing, Transwell/scratch healing assay, murine lung metastasis model Frontiers of medicine Medium 41454078
2025 HRASLS2 interacts with ASPH protein (co-immunoprecipitation) and increases ASPH protein stability; ASPH overexpression reverses the inhibitory effects of HRASLS2 knockdown on pancreatic cancer cell growth and glycolysis, placing ASPH downstream of HRASLS2 in a stability-dependent pathway. Co-immunoprecipitation, HRASLS2 knockdown and ASPH overexpression rescue, cell growth and glycolysis assays (glucose consumption, lactate, ECAR), xenograft model Naunyn-Schmiedeberg's archives of pharmacology Medium 40833600

Source papers

Stage 0 corpus · 70 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 The BAH domain of ORC1 links H4K20me2 to DNA replication licensing and Meier-Gorlin syndrome. Nature 285 22398447
2011 Structural basis of silencing: Sir3 BAH domain in complex with a nucleosome at 3.0 Å resolution. Science (New York, N.Y.) 208 22096199
1999 Two functionally distinct forms of the RSC nucleosome-remodeling complex, containing essential AT hook, BAH, and bromodomains. Molecular cell 182 10619019
1999 The BAH (bromo-adjacent homology) domain: a link between DNA methylation, replication and transcriptional regulation. FEBS letters 161 10100640
2000 Aspartyl beta -hydroxylase (Asph) and an evolutionarily conserved isoform of Asph missing the catalytic domain share exons with junctin. The Journal of biological chemistry 96 10956665
2018 Polycomb-mediated gene silencing by the BAH-EMF1 complex in plants. Nature genetics 84 30082786
2020 BAHCC1 binds H3K27me3 via a conserved BAH module to mediate gene silencing and oncogenesis. Nature genetics 80 33139953
2019 ASPH-notch Axis guided Exosomal delivery of Prometastatic Secretome renders breast Cancer multi-organ metastasis. Molecular cancer 77 31694640
2006 The BAH domain facilitates the ability of human Orc1 protein to activate replication origins in vivo. The EMBO journal 74 17066079
2012 Structure and function of the BAH domain in chromatin biology. Critical reviews in biochemistry and molecular biology 68 23181513
2014 Mutations in ASPH cause facial dysmorphism, lens dislocation, anterior-segment abnormalities, and spontaneous filtering blebs, or Traboulsi syndrome. American journal of human genetics 59 24768550
2006 Structure and function of the Saccharomyces cerevisiae Sir3 BAH domain. Molecular and cellular biology 54 16581798
2008 beta-Hydroxylation of the aspartyl residue in the phytotoxin syringomycin E: characterization of two candidate hydroxylases AspH and SyrP in Pseudomonas syringae. Biochemistry 53 18826255
2018 Hydroxylase Activity of ASPH Promotes Hepatocellular Carcinoma Metastasis Through Epithelial-to-Mesenchymal Transition Pathway. EBioMedicine 51 29764768
2018 BAH domains and a histone-like motif in DNA methyltransferase 1 (DNMT1) regulate de novo and maintenance methylation in vivo. The Journal of biological chemistry 49 30341171
1994 Activity of hemorrhagic metalloproteinase BaH-1 and myotoxin II from Bothrops asper snake venom on capillary endothelial cells in vitro. Toxicon : official journal of the International Society on Toxinology 47 8053003
2001 The BAH domain, polybromo and the RSC chromatin remodelling complex. Gene 39 11368894
2018 Recent advances in research on aspartate β-hydroxylase (ASPH) in pancreatic cancer: A brief update. Bosnian journal of basic medical sciences 38 30179586
2009 Mutational analysis of the Sir3 BAH domain reveals multiple points of interaction with nucleosomes. Molecular and cellular biology 37 19273586
2020 Evolutionarily ancient BAH-PHD protein mediates Polycomb silencing. Proceedings of the National Academy of Sciences of the United States of America 34 32393638
2021 CircTM7SF3 contributes to oxidized low-density lipoprotein-induced apoptosis, inflammation and oxidative stress through targeting miR-206/ASPH axis in atherosclerosis cell model in vitro. BMC cardiovascular disorders 31 33526034
2019 Structure and function of the Orc1 BAH-nucleosome complex. Nature communications 31 31263106
2013 The BAH domain of Rsc2 is a histone H3 binding domain. Nucleic acids research 31 23907388
2020 HMGA2 regulates circular RNA ASPH to promote tumor growth in lung adenocarcinoma. Cell death & disease 26 32719345
2016 Aspartate-β-hydroxylase (ASPH): A potential therapeutic target in human malignant gliomas. Heliyon 26 27981247
2021 A conserved BAH module within mammalian BAHD1 connects H3K27me3 to Polycomb gene silencing. Nucleic acids research 25 33823544
2011 Inactivation of Snt2, a BAH/PHD-containing transcription factor, impairs pathogenicity and increases autophagosome abundance in Fusarium oxysporum. Molecular plant pathology 24 21535351
2006 Structure of the Sir3 protein bromo adjacent homology (BAH) domain from S. cerevisiae at 1.95 A resolution. Protein science : a publication of the Protein Society 21 16641491
2005 Crystal structure of the proximal BAH domain of the polybromo protein. The Biochemical journal 21 15839835
2019 Loss of ciliary zonule protein hydroxylation and lens stability as a predicted consequence of biallelic ASPH variation. Ophthalmic genetics 20 30600741
2017 Ethanol-Induced White Matter Atrophy Is Associated with Impaired Expression of Aspartyl-Asparaginyl-β-Hydroxylase (ASPH) and Notch Signaling in an Experimental Rat Model. Journal of drug and alcohol research 20 29204305
2020 ASPH Regulates Osteogenic Differentiation and Cellular Senescence of BMSCs. Frontiers in cell and developmental biology 17 33015050
2022 INPP5F translocates into cytoplasm and interacts with ASPH to promote tumor growth in hepatocellular carcinoma. Journal of experimental & clinical cancer research : CR 16 34996491
2022 Traboulsi syndrome caused by mutations in ASPH: An autosomal recessive disorder with overlapping features of Marfan syndrome. European journal of medical genetics 16 35918038
2021 Upregulation of circ-ASPH contributes to glioma cell proliferation and aggressiveness by targeting the miR-599/AR/SOCS2-AS1 signaling pathway. Oncology letters 16 33777211
2015 The BAH domain of BAF180 is required for PCNA ubiquitination. Mutation research 16 26117423
2019 Traboulsi syndrome due to ASPH mutation: an under-recognised cause of ectopia lentis. Clinical dysmorphology 15 31274573
2024 Unusual catalytic strategy by non-heme Fe(ii)/2-oxoglutarate-dependent aspartyl hydroxylase AspH. Chemical science 14 38455014
2009 Caenorhabditis elegans BAH-1 is a DUF23 protein expressed in seam cells and required for microbial biofilm binding to the cuticle. PloS one 14 19707590
2022 Variants in ASPH cause exertional heat illness and are associated with malignant hyperthermia susceptibility. Nature communications 11 35697689
2020 Whole-exome sequencing identified a novel homozygous ASPH frameshift variant causing Traboulsi syndrome in a Chinese family. Molecular genetics & genomic medicine 10 33217155
2019 miR-135a acts as a tumor suppressor by targeting ASPH in endometrial cancer. International journal of clinical and experimental pathology 10 31934181
2014 Evaluation of HAAH/humbug quantitative detection in the diagnosis of hepatocellular carcinoma. Oncology reports 10 25394783
2020 A novel mutation in the aspartate beta-hydroxylase (ASPH) gene is associated with a rare form of Traboulsi syndrome. Ophthalmic genetics 9 33251883
2021 Expanding the clinical spectrum and management of Traboulsi syndrome: report on two siblings homozygous for a novel pathogenic variant in ASPH. Ophthalmic genetics 8 34018898
2024 ASPH dysregulates cell death and induces chemoresistance in hepatocellular carcinoma. Cancer letters 6 39706251
1998 Charge Delocalization in Persistent Benz[a]anthracenium Cations BAH(+) and Related alpha-Carbocations/Carboxonium Ions: Modeling Epoxide Ring Opening in Potent Carcinogens. The Journal of organic chemistry 6 11672371
2024 Genotype-phenotype profile of global ASPH-associated ectopia lentis and clinical findings from a Chinese cohort. Gene 5 38788814
2023 Inhibition of circular RNA ASPH reduces the proliferation and promotes the apoptosis of hepatic stellate cells in hepatic fibrosis. Biochemical pharmacology 5 36758707
2024 Effects of Clinical Mutations in the Second Coordination Sphere and Remote Regions on the Catalytic Mechanism of Non-Heme Fe(II)/2-Oxoglutarate-Dependent Aspartyl Hydroxylase AspH. Chemphyschem : a European journal of chemical physics and physical chemistry 4 38839574
2024 Circ_0005699 Expedites ox-LDL-Triggered Endothelial Cell Injury via Targeting miR-384/ASPH Axis. Cardiovascular toxicology 4 38976139
2021 Aspartate β-Hydroxylase (ASPH) Expression in Acute Myeloid Leukemia: A Potential Novel Therapeutic Target. Frontiers in oncology 4 35004304
2013 Control not at initiation? Bah, humbug! The EMBO journal 4 24363142
2025 ASPH Is a Metastatic Factor and Therapeutic Target in Chondrosarcoma. Cancers 3 40149287
2023 Aspartate β-hydroxylase (ASPH) Accelerates Intrahepatic Cholangiocarcinoma Metastasis via Upregulating SHH Signaling Pathway. Current protein & peptide science 3 37132101
2023 Traboulsi syndrome without features of Marfan syndrome caused by a novel homozygous ASPH variant associated with a heterozygous FBN1 variant. Ophthalmic genetics 2 37133842
2021 Growth optimization and identification of an ω-transaminase by a novel native PAGE activity staining method in a Bacillus sp. strain BaH isolated from Iranian soil. AMB Express 2 33759017
2021 The Trithorax group protein ASH1 requires a combination of BAH domain and AT hooks, but not the SET domain, for mitotic chromatin binding and survival. Chromosoma 2 34331109
2018 [Expression of ASPH Gene in Invasive Breast Cancer and Its Clinical Significance in Promoter Methylation]. Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 2 29737090
2018 Periodic Trends Manifested through Gas-Phase Generation of Anions Such as [AlH4]-, [GaH4]-, [InH4]-, [SrH3]-, [BaH3]-, [Ba(0)(η2-O2CH)1]-, [Pb(0)H]-, [Bi(I)H2]-, and Bi- from Formates. ACS omega 2 31458596
2010 [The distribution and expression pro-files of Aspartyl/Asparaginyl beta-hydroxylase (ASPH) in some tumorous cell lines and tissues]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 2 20230674
2025 HRASLS2 promotes the growth and glycolysis of pancreatic cancer by enhancing the stability of ASPH. Naunyn-Schmiedeberg's archives of pharmacology 1 40833600
2025 Multi-omics integration identifies ASPH and PTTG1 as potential causal drivers of lung adenocarcinoma progression and immune evasion. Frontiers in immunology 1 41312363
2024 PHD-BAH Domain in ASH1L Could Recognize H3K4 Methylation and Regulate the Malignant Behavior of Cholangiocarcinoma. Anti-cancer agents in medicinal chemistry 1 39034728
2026 Enteroviral epitope mimicry enables NK cell-mediated targeting of ASPH in hepatocellular carcinoma. bioRxiv : the preprint server for biology 0 41993253
2025 Opposite Effects of Added AsPh3 Reveal a Drastic Mechanistic Switch in RhI/AuI Transmetalations via Rh-Au Bonded Intermediates. Inorganic chemistry 0 40571906
2025 ASPH interacts with RUVBL2 to promote tumor metastasis in lung adenocarcinoma via MAPK and Notch signaling pathways. Frontiers of medicine 0 41454078
2022 The inhibitory effect of human umbilical cord mesenchymal stem cells expressing anti-HAAH scFv-sTRAIL fusion protein on glioma. Frontiers in bioengineering and biotechnology 0 36425649
2010 [Cloning of the variable region genes from hybridoma against HAAH and then construction and expression of anti-HAAH scFv]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 0 20423655
2002 [Atomic force microscopic observation of the neurons membrane in primary culture after treatment with N-Methyl-D-Asph]. Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA 0 12433625

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