Affinage

DCPS

m7GpppX diphosphatase · UniProt Q96C86

Length
337 aa
Mass
38.6 kDa
Annotated
2026-06-09
56 papers in source corpus 19 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/7 claims corpus-supported (86%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DCPS (DcpS) is a HIT-family scavenger decapping pyrophosphatase that completes eukaryotic mRNA turnover by hydrolyzing the residual cap structure left after exonucleolytic decay (PMID:12198172). It specifically cleaves the methylated cap (m7GpppN) but not unmethylated cap or intact capped RNA, with a central HIT-motif histidine essential for catalysis (PMID:12198172), and it also converts m7GDP—the product of Dcp2 decapping in the 5'-to-3' pathway—into m7GMP, making cap catabolism a pathway-independent endpoint conserved in yeast and human (PMID:14523240). Catalysis is governed by a domain-swapped dimer: cap binding produces an asymmetric open/closed dimer in which Tyr273 drives conformational change and product release (PMID:15769464), the two cap sites operate in a dynamic, mutually exclusive manner whose rate is tuned by substrate concentration (PMID:18441014), and steric clashes with the third nucleotide of a capped fragment restrict activity to substrates shorter than three nucleotides, a length-sensing mechanism conserved from yeast to humans (PMID:32723815). Beyond catalysis, DcpS is a nucleocytoplasmic shuttling protein with separable nuclear import and CRM1-dependent export signals that modulates cap-proximal pre-mRNA splicing by displacing the nuclear cap-binding protein Cbp20 from cap structures (PMID:18426921), and it promotes microRNA and selective transcript turnover by acting with the 5'-to-3' exonucleases XRN1/XRN2 independently of its decapping activity (PMID:23541767, PMID:26584588, PMID:26001796). In human disease, loss-of-function DCPS mutations abolish decapping activity and cause a neurodevelopmental disorder affecting cognition (PMID:25701870, PMID:25712129); the resulting neuronal phenotypes—impaired radial migration, neurite outgrowth, and differentiation (PMID:34467373)—are linked to a creatine deficiency arising from reduced GAMT expression that can be reversed by creatine supplementation (PMID:40410278). DcpS additionally supports P-body integrity, and its reduction restores RNA turnover and neuronal survival in TDP-43 proteinopathy (PMID:41943580). Its catalytic pocket is pharmacologically tractable: C5-substituted quinazolines trap the enzyme in an inactive open conformation (PMID:18839960).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2002 High

    Established the biochemical identity of DcpS as a scavenger decapping enzyme, answering what hydrolyzes the residual cap and defining the first functional HIT-family member.

    Evidence Protein purification, recombinant expression, in vitro decapping assays with cap analogs, and HIT-motif histidine mutagenesis

    PMID:12198172

    Open questions at the time
    • Did not resolve dimeric architecture or catalytic mechanism
    • In vivo substrate scope not defined
  2. 2003 High

    Extended DcpS function from the 3'-to-5' pathway to the 5'-to-3' pathway by showing it converts the Dcp2 product m7GDP to m7GMP, making cap catabolism a general decay endpoint.

    Evidence In vitro decapping assays in human and yeast extracts with reaction-intermediate identification and fractionation

    PMID:14523240

    Open questions at the time
    • Did not place the reaction in a complete cap catabolism pathway
    • Physiological balance between pathways not quantified
  3. 2003 Medium

    Characterized the C. elegans ortholog DCS-1 as a Hint-branch nucleotide hydrolase with m7G specificity and an unexpected interaction with flavin reductase NR1, hinting at functions beyond cap hydrolysis.

    Evidence Fluorescent 7meGpppBODIPY substrate kinetics, co-immunoprecipitation, and immunocytochemistry in COS cells

    PMID:12871939

    Open questions at the time
    • NR1 interaction not mechanistically connected to decapping
    • Localization to perinuclear structure not defined
  4. 2005 High

    Provided the structural basis for cap recognition, showing apo-DcpS is a symmetric dimer that becomes asymmetric on cap binding with Tyr273 driving conformational change.

    Evidence X-ray crystallography of apo and m7GDP-bound DcpS with mutagenesis and decapping assays

    PMID:15769464

    Open questions at the time
    • Did not establish catalytic kinetics of the two-site mechanism
    • Substrate length discrimination not addressed
  5. 2008 High

    Defined the catalytic kinetics of the dimer, showing the two cap sites operate in a dynamic, mutually exclusive manner regulated by substrate concentration.

    Evidence Transient-state (stopped-flow) kinetic analysis interpreted against structural data

    PMID:18441014

    Open questions at the time
    • Did not connect kinetics to in vivo decay rates
    • Regulatory significance of substrate-tuning unclear
  6. 2008 High

    Revealed a nuclear, decapping-dependent role in splicing, answering whether DcpS has functions beyond cap clearance by linking it to Cbp20 displacement at cap-proximal introns.

    Evidence shRNA knockdown, import/export signal mapping, in vitro cap-binding displacement, reporter splicing assays, and Cbp20 rescue

    PMID:18426921

    Open questions at the time
    • Mechanism of Cbp20 competition in vivo not fully resolved
    • Genome-wide splicing impact not quantified
  7. 2008 High

    Identified DcpS as a druggable target of C5-substituted quinazolines that trap it in an inactive open state, linking inhibition to SMN2 induction.

    Evidence Protein microarray binding with radiolabeled probe, in vitro decapping inhibition, and structural conformational analysis

    PMID:18839960

    Open questions at the time
    • Mechanistic link between DcpS inhibition and SMN2 induction not established
    • Off-target effects of quinazolines not excluded
  8. 2013 High

    Uncovered a catalytic-independent function in microRNA turnover via direct cooperation with XRN-1, separating two distinct molecular activities of the enzyme.

    Evidence C. elegans dcs-1 genetic analysis, interaction studies, and miRNA level measurements with function-separation assays

    PMID:23541767

    Open questions at the time
    • Mechanism by which DCS-1 stimulates XRN-1 unresolved
    • Conservation to mammals not shown in this study
  9. 2014 Medium

    Reconstituted a complete cap catabolism pathway, placing DcpS alongside Aph1/FHIT and nucleoside diphosphate kinase in m7GDP elimination.

    Evidence In vitro biochemical assays and pathway reconstitution in yeast and human extracts

    PMID:25432955

    Open questions at the time
    • In vivo flux through the reconstituted pathway not measured
    • Relative contributions of DcpS and FHIT unclear
  10. 2015 Medium

    Confirmed the conserved catalytic-independent miRNA turnover role in human cells and assigned it to the cytoplasm via Xrn2 dependency.

    Evidence Human DcpS knockdown, miRNA measurements, subcellular fractionation, and decapping-dead mutant analysis

    PMID:26584588

    Open questions at the time
    • Direct DcpS-Xrn2 physical interaction not biochemically defined
    • Single-lab observation
  11. 2015 Medium

    Showed transcript-selective RNA stability control by DcpS with XRN1, identifying lncRNAs DRNT1/DRNT2 as responsive transcripts.

    Evidence RG3039 inhibitor treatment, global mRNA profiling, stability assays, catalytic mutant complementation, and Xrn1 knockdown co-dependence

    PMID:26001796

    Open questions at the time
    • Basis of transcript selectivity unknown
    • Direct vs indirect effects on DRNT transcripts not separated
  12. 2015 High

    Established human disease relevance by showing loss-of-function DCPS mutations abolish decapping activity and are required for normal neurodevelopment and cognition.

    Evidence Patient cells with homozygous DCPS mutations and in vitro decapping assays on m7G cap derivatives (replicated across two publications)

    PMID:25701870 PMID:25712129

    Open questions at the time
    • Downstream molecular cause of neurodevelopmental phenotype not defined in this study
    • Whether catalytic or non-catalytic function drives disease unclear here
  13. 2018 Medium

    Linked DcpS to spliceosome physical interactions and pre-mRNA mis-splicing in cancer, providing a basis for its anti-leukemic vulnerability.

    Evidence Genome-wide CRISPR-Cas9 screen, co-IP mass spectrometry interactome, and RG3039 transcriptomic splicing analysis in AML cells

    PMID:29478914

    Open questions at the time
    • Which spliceosome interactions are direct not resolved
    • Causal step from DcpS loss to mis-splicing unclear
  14. 2020 High

    Defined the substrate length-sensing mechanism, explaining selectivity for fragments shorter than three nucleotides via steric clashes at the active site.

    Evidence Methyl-TROSY NMR, X-ray crystallography, mutagenesis, and in vitro assays with varying-length substrates

    PMID:32723815

    Open questions at the time
    • Physiological consequence of relaxing length specificity not tested
    • Does not address non-catalytic functions
  15. 2022 Medium

    Demonstrated that DcpS loss impairs neuronal migration, polarity, neurite outgrowth, and identity, connecting enzyme function to cortical development.

    Evidence In utero electroporation knockdown in mouse neocortex and patient-derived human neuron morphology/marker analysis

    PMID:34467373

    Open questions at the time
    • Molecular mediators of the migration defect not identified
    • Catalytic vs non-catalytic requirement not dissected
  16. 2022 Low

    Validated DcpS as a degradable drug target by achieving rapid VHL-mediated PROTAC degradation that is anti-proliferative in AML.

    Evidence PROTAC (JCS-1) design with western blot degradation and viability assays in AML lines

    PMID:35749470

    Open questions at the time
    • Limited mechanistic depth on DcpS biology
    • Whether anti-proliferative effect reflects catalytic loss or scaffolding loss untested
  17. 2025 Medium

    Identified a metabolic mechanism for the neurodevelopmental phenotype: DcpS mutation reduces GAMT expression causing creatine deficiency, reversible by creatine supplementation.

    Evidence Metabolomics of patient-derived cells, iPSC neuronal differentiation, GAMT mRNA/protein quantification, and creatine rescue

    PMID:40410278

    Open questions at the time
    • How DcpS loss specifically lowers GAMT mRNA not mechanistically defined
    • Single-lab finding
  18. 2025 Medium

    Positioned DcpS as a modifier of P-body function in TDP-43 proteinopathy, where its reduction restores RNA turnover and neuronal survival.

    Evidence CRISPRi screening in human neurons, P-body imaging, RNA decay assays, and survival measurements

    PMID:41943580

    Open questions at the time
    • Molecular basis of DcpS effect on P-body integrity unresolved
    • Generalizability beyond TDP-43 LOF context untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how DcpS partitions between its catalytic decapping role and its catalytic-independent scaffolding roles (XRN cofactor, splicing, P-body regulation) to produce its developmental and disease phenotypes.
  • No unified model linking catalytic vs non-catalytic functions to neurodevelopmental disease
  • Mechanism connecting cap clearance to GAMT/creatine and P-body regulation unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016787 hydrolase activity 5 GO:0003723 RNA binding 4 GO:0140098 catalytic activity, acting on RNA 3
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 2
Pathway
R-HSA-8953854 Metabolism of RNA 5 R-HSA-74160 Gene expression (Transcription) 2
Partners
CBP20FHITXRN1XRN2

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 DcpS was identified as a scavenger mRNA decapping pyrophosphatase that specifically hydrolyzes methylated cap analog (m7GpppN) but not unmethylated cap analog and does not act on intact capped RNA. The central histidine within the HIT motif is critical for decapping activity, defining DcpS as the first HIT-family member with a defined biological function. Protein purification from mammalian cells, recombinant protein expression, in vitro decapping assays with cap analogs, site-directed mutagenesis of HIT motif histidines The EMBO journal High 12198172
2003 DcpS can also function in the 5'-3' mRNA decay pathway by converting m7GDP (the product of Dcp2 decapping) to m7GMP, in addition to its established role in the 3'-5' pathway. This activity was identified in both yeast and human, making m7GMP a general pathway-independent by-product of eukaryotic mRNA decay. In vitro decapping assays in human cell extracts and yeast, biochemical identification of reaction intermediates and products, fractionation to identify the responsible factor as DcpS Proceedings of the National Academy of Sciences of the United States of America High 14523240
2005 Crystal structures of human DcpS in ligand-free and m7GDP-bound forms revealed that apo-DcpS is a symmetric dimer, while cap-analog-bound DcpS is an asymmetric dimer with one site open and one closed. Tyr273 in the cap-binding pocket undergoes conformational changes upon cap binding and plays an important role in cap binding and product release, as demonstrated by mutagenesis. X-ray crystallography, site-directed mutagenesis, biochemical decapping assays Journal of molecular biology High 15769464
2008 DcpS is a nucleocytoplasmic shuttling protein containing separable nuclear import and CRM1-dependent export signals. Reduction of DcpS levels via shRNA impaired cap-proximal intron splicing of reporter and endogenous genes. DcpS efficiently displaced the nuclear cap-binding protein Cbp20 from cap structure, and complementation with Cbp20 reversed the splicing defect, indicating DcpS modulates splicing through Cbp20. shRNA knockdown, immunofluorescence, nuclear import/export signal mapping, in vitro cap-binding displacement assays, reporter splicing assays, rescue by Cbp20 complementation RNA (New York, N.Y.) High 18426921
2008 DcpS inhibition by C5-substituted quinazolines holds the enzyme in an open, catalytically incompetent conformation. These compounds potently inhibit DcpS decapping activity with potency correlating with SMN2 promoter induction. DcpS was identified as the binding target using protein microarray scanning with a radiolabeled quinazoline probe. Protein microarray binding with radiolabeled probe, in vitro DcpS decapping activity assays, structural analysis of inhibitor-bound conformation ACS chemical biology High 18839960
2008 Transient state kinetic studies established that DcpS has a dynamic and mutually exclusive cap hydrolysis activity at the two cap binding sites of its dimer. The rate-limiting step and rate of decapping are regulated by cap substrate concentration; decapping is highly efficient at low cap substrate concentrations but regulated (slowed) with excess substrate, reflecting the domain-swapped dimeric architecture. Transient state kinetic analysis (stopped-flow), mechanistic interpretation based on structural data The Journal of biological chemistry High 18441014
2013 The C. elegans DcpS ortholog DCS-1 interacts with the 5'-3' exonuclease XRN-1 to promote microRNA degradation in a manner independent of its decapping scavenger activity, establishing two distinct molecular functions for DCS-1. Loss of dcs-1 increases functional microRNA levels. Genetic analysis in C. elegans (dcs-1 mutants), protein interaction studies, microRNA level measurements, functional assays separating decapping from XRN-1 cofactor activity Molecular cell High 23541767
2015 Human DcpS conserves a role in miRNA turnover, functioning as a nucleocytoplasmic shuttling protein that activates miRNA degradation independently of its scavenger decapping activity in the cytoplasmic compartment. This function requires the 5'-3' exonuclease Xrn2. DcpS knockdown in human cells, miRNA level measurements, subcellular fractionation, decapping-dead mutant analysis to separate functions, Xrn2 co-dependency assays Scientific reports Medium 26584588
2015 Loss-of-function mutations in DCPS (splice site and missense variants) abolish decapping activity as shown by in vitro decapping assays with m7G cap derivatives, establishing that DCPS enzymatic activity is required for normal neurological development and cognition in humans. Patient cells with homozygous DCPS mutations, in vitro decapping assays using m7G cap derivatives as substrates Human molecular genetics High 25701870 25712129
2015 DcpS, in conjunction with Xrn1, regulates RNA stability in a transcript-selective manner in mammalian cells. Two long non-coding RNAs (DRNT1 and DRNT2) were identified as DcpS-responsive transcripts; DRNT1 stability increased upon DcpS inhibition (RG3039) in a manner dependent on both DcpS catalytic activity and Xrn1. DcpS inhibitor treatment (RG3039), global mRNA profiling, targeted RNA stability assays, catalytic mutant complementation, Xrn1 knockdown co-dependence RNA (New York, N.Y.) Medium 26001796
2018 DCPS interacts with components of pre-mRNA metabolic pathways including spliceosomes, as revealed by mass spectrometry co-immunoprecipitation in AML cells. DCPS inhibition (RG3039) induces pre-mRNA mis-splicing, contributing to anti-leukemic activity. Genome-wide CRISPR-Cas9 screen, mass spectrometry after co-immunoprecipitation to identify DCPS interactors, RG3039 treatment with transcriptomic analysis of splicing changes Cancer cell Medium 29478914
2020 DcpS only processes mRNA fragments shorter than three nucleotides. Using NMR (methyl-TROSY) and X-ray crystallography, steric clashes between the enzyme and the third nucleotide of capped mRNA prevent conformational changes required for a catalytically competent active site. Point mutations enlarging the space for the third nucleotide enhance activity on longer substrates. This substrate length-sensing mechanism is conserved from yeast to humans. Methyl-TROSY NMR spectroscopy, X-ray crystallography, site-directed mutagenesis, in vitro enzymatic assays with substrates of varying length Proceedings of the National Academy of Sciences of the United States of America High 32723815
2022 DcpS is required for radial migration, polarity, neurite outgrowth, and identity of developing glutamatergic neurons in the mouse neocortex, as shown by loss-of-function studies. Human neurons derived from DcpS mutation patients showed compromised differentiation and neurite outgrowth. In utero electroporation knockdown in mouse neocortex, patient-derived human neurons, morphological and marker analysis Cerebral cortex (New York, N.Y. : 1991) Medium 34467373
2025 DcpS loss reduces P-body integrity, and reducing DCPS in human neurons with TDP-43 loss-of-function restores P-body function and RNA turnover, improving neuronal survival. TDP-43 LOF hyperactivates P-bodies, increasing mRNA association and RNA decay, and DCPS acts as a genetic modifier of this pathway. CRISPRi screening in human neurons, P-body imaging, RNA decay assays, neuronal survival measurements Neuron Medium 41943580
2025 DcpS mutant patient-derived cells harbor creatine deficiency and elevated guanidinoacetate (GAA) due to reduced mRNA and protein levels of guanidinoacetate methyltransferase (GAMT). Creatine supplementation reversed compromised neurogenesis and neurite outgrowth during differentiation of DcpS mutant iPSCs into neurons. Metabolomics of patient-derived cells, iPSC differentiation assays, creatine supplementation rescue experiments, GAMT mRNA/protein quantification Scientific reports Medium 40410278
2014 In yeast and human extracts, m7GpppN cap dinucleotides can be degraded through a pathway involving DcpS together with Aph1/FHIT. DcpS acts in concert with NTPs and nucleoside diphosphate kinase for m7GDP elimination, establishing a complete cap catabolism pathway. In vitro biochemical assays in yeast and human extracts, identification and characterization of Aph1/FHIT as a new scavenger decapping enzyme, pathway reconstitution Nucleic acids research Medium 25432955
2003 C. elegans DCS-1 is a member of the Hint branch of the histidine triad superfamily of nucleotide hydrolases with low micromolar specificity for 7-methylguanosine ribonucleotides; trimethylated G substrates are poor competitors. DCS-1 localizes to the nucleus and a perinuclear structure and binds to and directly modulates the activity of the flavin reductase NR1. Novel fluorescent substrate assay (7meGpppBODIPY), enzyme kinetics, co-immunoprecipitation, immunocytochemistry in COS cells The Journal of biological chemistry Medium 12871939
2022 A PROTAC (JCS-1) that recruits VHL E3 ligase to DcpS causes potent, rapid, and sustained DcpS protein degradation at nanomolar concentrations in AML cell lines, validating DcpS as a druggable target whose depletion is anti-proliferative in AML. PROTAC design, western blot for DcpS degradation, cell viability assays in AML lines ACS chemical biology Low 35749470

Source papers

Stage 0 corpus · 56 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 The scavenger mRNA decapping enzyme DcpS is a member of the HIT family of pyrophosphatases. The EMBO journal 218 12198172
1992 Multiple domains of the RNA polymerase I activator hUBF interact with the TATA-binding protein complex hSL1 to mediate transcription. Genes & development 153 1398072
2006 Phosphorylation of Hsl1 by Hog1 leads to a G2 arrest essential for cell survival at high osmolarity. The EMBO journal 117 16688223
2008 Synthesis and characterization of mRNA cap analogs containing phosphorothioate substitutions that bind tightly to eIF4E and are resistant to the decapping pyrophosphatase DcpS. RNA (New York, N.Y.) 111 18430890
2018 Genome-wide CRISPR-Cas9 Screen Identifies Leukemia-Specific Dependence on a Pre-mRNA Metabolic Pathway Regulated by DCPS. Cancer cell 101 29478914
2008 DcpS as a therapeutic target for spinal muscular atrophy. ACS chemical biology 101 18839960
2004 In Candida albicans, the Nim1 kinases Gin4 and Hsl1 negatively regulate pseudohypha formation and Gin4 also controls septin organization. The Journal of cell biology 86 14769857
2013 The DcpS inhibitor RG3039 improves survival, function and motor unit pathologies in two SMA mouse models. Human molecular genetics 72 23736298
2003 DcpS can act in the 5'-3' mRNA decay pathway in addition to the 3'-5' pathway. Proceedings of the National Academy of Sciences of the United States of America 72 14523240
2001 GSK-3 kinase Mck1 and calcineurin coordinately mediate Hsl1 down-regulation by Ca2+ in budding yeast. The EMBO journal 68 11230131
2005 Caenorhabditis elegans decapping proteins: localization and functional analysis of Dcp1, Dcp2, and DcpS during embryogenesis. Molecular biology of the cell 57 16207815
2013 The DcpS inhibitor RG3039 improves motor function in SMA mice. Human molecular genetics 54 23727836
2004 Nematode m7GpppG and m3(2,2,7)GpppG decapping: activities in Ascaris embryos and characterization of C. elegans scavenger DcpS. RNA (New York, N.Y.) 48 15383679
2013 The decapping scavenger enzyme DCS-1 controls microRNA levels in Caenorhabditis elegans. Molecular cell 47 23541767
2005 Crystal structures of human DcpS in ligand-free and m7GDP-bound forms suggest a dynamic mechanism for scavenger mRNA decapping. Journal of molecular biology 44 15769464
2022 HSL1 and BAM1/2 impact epidermal cell development by sensing distinct signaling peptides. Nature communications 43 35169143
2006 Enzymatically stable 5' mRNA cap analogs: synthesis and binding studies with human DcpS decapping enzyme. Bioorganic & medicinal chemistry 43 16431118
2015 Mutations in DCPS and EDC3 in autosomal recessive intellectual disability indicate a crucial role for mRNA decapping in neurodevelopment. Human molecular genetics 42 25701870
2014 Elimination of cap structures generated by mRNA decay involves the new scavenger mRNA decapping enzyme Aph1/FHIT together with DcpS. Nucleic acids research 41 25432955
2008 DcpS scavenger decapping enzyme can modulate pre-mRNA splicing. RNA (New York, N.Y.) 36 18426921
2014 Decapping Scavenger (DcpS) enzyme: advances in its structure, activity and roles in the cap-dependent mRNA metabolism. Biochimica et biophysica acta 34 24742626
2008 DcpS, a general modulator of cap-binding protein-dependent processes? RNA biology 34 18948758
2003 Coordinate expression of NADPH-dependent flavin reductase, Fre-1, and Hint-related 7meGMP-directed hydrolase, DCS-1. The Journal of biological chemistry 33 12871939
2015 Loss of the scavenger mRNA decapping enzyme DCPS causes syndromic intellectual disability with neuromuscular defects. Human molecular genetics 30 25712129
2007 DCS-1, DCS-2, and DFV share amino acid substitutions at the extracellular RhD protein vestibule. Transfusion 23 17900276
2009 APC/CCdh1 specific degradation of Hsl1 and Clb2 is required for proper stress responses of S. cerevisiae. Cell cycle (Georgetown, Tex.) 21 19713762
2008 Mechanistic and kinetic analysis of the DcpS scavenger decapping enzyme. The Journal of biological chemistry 21 18441014
2019 The yeast scavenger decapping enzyme DcpS and its application for in vitro RNA recapping. Scientific reports 20 31197197
2015 DcpS is a transcript-specific modulator of RNA in mammalian cells. RNA (New York, N.Y.) 20 26001796
2015 The human decapping scavenger enzyme DcpS modulates microRNA turnover. Scientific reports 19 26584588
2008 Proteomic approach to the identification of novel delta-lactoferrin target genes: Characterization of DcpS, an mRNA scavenger decapping enzyme. Biochimie 19 18725266
2016 Coordinate action of distinct sequence elements localizes checkpoint kinase Hsl1 to the septin collar at the bud neck in Saccharomyces cerevisiae. Molecular biology of the cell 17 27193302
2017 Design of Potent mRNA Decapping Scavenger Enzyme (DcpS) Inhibitors with Improved Physicochemical Properties To Investigate the Mechanism of Therapeutic Benefit in Spinal Muscular Atrophy (SMA). Journal of medicinal chemistry 15 28257199
2020 Molecular basis of the selective processing of short mRNA substrates by the DcpS mRNA decapping enzyme. Proceedings of the National Academy of Sciences of the United States of America 14 32723815
2023 Ferroptosis induced by DCPS depletion diminishes hepatic metastasis in uveal melanoma. Biochemical pharmacology 13 37245534
2017 In vitro and in vivo effects of 2,4 diaminoquinazoline inhibitors of the decapping scavenger enzyme DcpS: Context-specific modulation of SMN transcript levels. PloS one 13 28945765
2010 Structural requirements for Caenorhabditis elegans DcpS substrates based on fluorescence and HPLC enzyme kinetic studies. The FEBS journal 13 20546305
2022 Targeted Degradation of mRNA Decapping Enzyme DcpS by a VHL-Recruiting PROTAC. ACS chemical biology 12 35749470
2020 Objective assessment of chronic pain in donkeys using the donkey chronic pain scale (DCPS): A scale-construction study. Veterinary journal (London, England : 1997) 11 33375958
2015 The effect of the DcpS inhibitor D156844 on the protective action of follistatin in mice with spinal muscular atrophy. Neuromuscular disorders : NMD 11 26055638
2018 An additional patient with a homozygous mutation in DCPS contributes to the delination of Al-Raqad syndrome. American journal of medical genetics. Part A 9 30289615
2015 A library approach to rapidly discover photoaffinity probes of the mRNA decapping scavenger enzyme DcpS. Molecular bioSystems 8 25959423
2024 Protein kinase Hsl1 phosphorylates Pah1 to inhibit phosphatidate phosphatase activity and regulate lipid synthesis in Saccharomyces cerevisiae. The Journal of biological chemistry 7 39009344
2022 mRNA-Decapping Associated DcpS Enzyme Controls Critical Steps of Neuronal Development. Cerebral cortex (New York, N.Y. : 1991) 6 34467373
2015 Effect of different N7 substitution of dinucleotide cap analogs on the hydrolytic susceptibility towards scavenger decapping enzymes (DcpS). Biochemical and biophysical research communications 5 26049109
2005 Role of a novel dual flavin reductase (NR1) and an associated histidine triad protein (DCS-1) in menadione-induced cytotoxicity. Biochemical and biophysical research communications 5 16140270
2024 Effect of the mRNA decapping enzyme scavenger (DCPS) inhibitor RG3039 on glioblastoma. Journal of translational medicine 4 39350123
2020 Leukoencephalopathy in Al-Raqad syndrome: Expanding the clinical and neuroimaging features caused by a biallelic novel missense variant in DCPS. American journal of medical genetics. Part A 4 32770650
2025 DCPS modulates TDP-43 mediated neurodegeneration through P-body regulation. bioRxiv : the preprint server for biology 2 40661462
2025 The first case of Al-Raqad syndrome in Japan is associated with a homozygous DCPS exonic variant resulting in aberrant splicing. Brain & development 1 40344930
2025 Creatine mitigates neurogenesis impairment caused by defective DcpS decapping. Scientific reports 1 40410278
2019 The natural antisense transcript NATTD regulates the transcription of decapping scavenger (DcpS) enzyme. The international journal of biochemistry & cell biology 1 30858142
2007 Kinetics of C. elegans DcpS cap hydrolysis studied by fluorescence spectroscopy. Nucleosides, nucleotides & nucleic acids 1 18066754
2026 Integrated FHIT and IDH2 biomarker profiling predicts lethal sensitivity to DCPS inhibition in Acute Myeloid Leukemia and Myelodysplastic syndrome. Discover oncology 0 41888450
2026 DCPS modulates TDP-43-linked neurodegeneration through P-body-mediated RNA decay. Neuron 0 41943580
2026 Liquid-liquid phase separation and the formation of amyloid fibrils from DcpS scavenger enzymes. Scientific reports 0 42204260

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