Affinage

NDST1

Bifunctional heparan sulfate N-deacetylase/N-sulfotransferase 1 · UniProt P52848

Length
882 aa
Mass
100.9 kDa
Annotated
2026-06-10
38 papers in source corpus 24 papers cited in narrative 25 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

NDST1 is a Golgi-resident bifunctional sulfotransferase that initiates heparan sulfate (HS) maturation by N-deacetylating and N-sulfating glucosamine residues, thereby controlling the sulfation code that governs HS-dependent growth factor and morphogen signaling during development (PMID:12590599, PMID:15253930). Its two activities are mechanistically coupled and ordered: active-site mutants that destroy N-deacetylase activity abolish N-sulfation, establishing N-deacetylation as the prerequisite, rate-limiting step, and the enzyme requires Mn²⁺ and uses PAPS as the sulfate donor (PMID:12590599, PMID:15253930). NDST1 is incorporated with the HS copolymerase machinery into a biosynthetic complex, interacting physically with EXT1 and EXT2, whose levels reciprocally modulate NDST1 abundance, glycosylation, and HS sulfation (PMID:18337501, PMID:35137078). Through the sulfation pattern it imposes, NDST1-modified HS sets the binding of HS to morphogens and growth factors and thereby tunes FGF (PMID:17107998, PMID:20502530), BMP (PMID:17376755, PMID:19299468), Hedgehog (PMID:16020517, PMID:20554886), Wnt/PCP (PMID:36726238, PMID:38326088), and VEGFA (PMID:23884416) signaling, acting positively or negatively depending on tissue context—serving as a co-receptor scaffold for FGF, while restricting and internalizing BMP and confining Hedgehog signaling to its proper zone (PMID:17107998, PMID:17376755, PMID:19299468, PMID:20554886). Consistent with these roles, Ndst1 loss in mice produces tissue-specific developmental defects across lung, brain, craniofacial structures, skeleton, mammary gland, vasculature, and kidney podocytes (PMID:10664446, PMID:16020517, PMID:20502530, PMID:20206635, PMID:23924956). In humans, recessive and compound-heterozygous NDST1 mutations cause intellectual disability, and the variant p.(Gly611Ser) abolishes N-sulfotransferase activity alone while sparing N-deacetylase activity, demonstrating that loss of N-sulfation is sufficient to cause cognitive impairment (PMID:25125150, PMID:28211985, PMID:38129107).

Mechanistic history

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

    Established the basic enzymology of NDST1 by quantifying its substrate preference and product inhibition, defining how it acts on partially modified HS.

    Evidence In vitro N-deacetylase and [3H]-acetate release assays on NDST1-transfected HEK293 lysates with defined substrates

    PMID:12634318

    Open questions at the time
    • Did not establish whether the two activities act on the same residue
    • Cofactor and donor requirements not addressed here
  2. 2003 High

    Resolved how the two catalytic activities are coupled, showing N-deacetylation is the obligatory rate-limiting step preceding N-sulfation.

    Evidence Active-site point mutagenesis of NDST1 in stable 293 cell lines with structural analysis of secreted HS

    PMID:12590599

    Open questions at the time
    • Mechanism by which two enzyme molecules cooperate on one glucosamine not structurally defined
    • No crystal structure of full-length enzyme
  3. 2004 High

    Defined the cofactor requirements and reconstituted both NDST1 activities, and genetically established the epistatic order of HS modification by showing 6-O-sulfation can proceed without N-sulfation.

    Evidence Recombinant rat NDST1 expressed in yeast plus NDST1/NDST2 double-knockout mouse ES cell HS structural analysis

    PMID:15253930 PMID:15319440

    Open questions at the time
    • Spatial organization of downstream enzymes relative to NDST1 not resolved
    • Redundancy between NDST isoforms in vivo not fully partitioned
  4. 2000 High

    First in vivo demonstration that NDST1-dependent HS sulfation is required for a specific developmental process—type II pneumocyte maturation.

    Evidence Gene-targeted Ndst1 knockout mice with lung morphology and lipid biochemistry

    PMID:10664446

    Open questions at the time
    • Which HS-dependent signaling pathway drives the lung phenotype not identified here
  5. 2005 Medium

    Placed Ndst1 upstream of morphogen pathways by linking its loss to Shh- and FGF-dependent craniofacial and neural development.

    Evidence Conditional Ndst1 knockout mice with phenotypic and signaling pathway analysis

    PMID:16020517

    Open questions at the time
    • Direct ligand-HS binding changes not measured in this study
    • Pathway-specific contributions not separated
  6. 2006 High

    Demonstrated tissue-specific pathway selectivity—Ndst1-modified HS is specifically required for FGF, but not BMP or Wnt, signaling in the lens.

    Evidence Lens-specific Ndst1 knockout with FGF-receptor binding assay and pERK/ERM readouts plus BMP/Wnt controls

    PMID:17107998

    Open questions at the time
    • Why FGF is selectively HS-dependent in this context not mechanistically explained
  7. 2007 High

    Showed NDST1-dependent HS can act as a negative modulator, restraining BMP-PTHrP signaling in endochondral ossification, and acts across FGF/Hedgehog/Wnt in development.

    Evidence Ndst1 knockout mice with in situ HS-binding assays, signaling Westerns, and noggin rescue

    PMID:17183530 PMID:17376755

    Open questions at the time
    • Molecular basis of positive vs negative modulation across tissues not unified
    • Mechanism of HS sequestration of BMP not structurally defined
  8. 2008 Medium

    Identified NDST1's physical incorporation into the HS biosynthetic machinery, with EXT2 stabilizing NDST1 and EXT1 opposing it.

    Evidence EXT1/EXT2 overexpression in HEK293, co-IP of EXT2-NDST1, and NDST activity in transgenic tissue

    PMID:18337501

    Open questions at the time
    • Interaction shown by single co-IP without reconstitution
    • Stoichiometry and architecture of the GAGosome unresolved
  9. 2010 High

    Extended the in vivo role to BMP internalization, mammary FGF-dependent morphogenesis, vascular remodeling, and Ihh topography, mapping context-specific functions.

    Evidence Multiple cell-type-specific Cre-loxP Ndst1 knockouts with ligand binding, internalization, proliferation, and signaling readouts

    PMID:19299468 PMID:20206635 PMID:20502530 PMID:20554886

    Open questions at the time
    • Tissue-specific HS sequence requirements not defined at structural resolution
    • Whether shared or distinct downstream effectors mediate each phenotype unclear
  10. 2013 Medium

    Connected NDST1 to upstream regulation (miR-24) and to VEGFA signaling, and established a specific role in podocyte organization.

    Evidence miR-24/siRNA knockdown in endothelial cells with VEGFA binding/chemotaxis assays; podocyte-specific Ndst1 knockout with EM

    PMID:23884416 PMID:23924956

    Open questions at the time
    • miR-24 regulation tested in single lab
    • Podocyte phenotype mechanism beyond HS sulfation loss not detailed
  11. 2014 Medium

    Linked NDST1 N-sulfotransferase activity to human cognition via recessive intellectual disability mutations clustered in the sulfotransferase domain.

    Evidence Human mutation analysis with structural modeling and Drosophila sulfateless RNAi long-term memory assay

    PMID:25125150

    Open questions at the time
    • Functional consequence of each human variant not directly assayed
    • Neuronal HS targets relevant to memory not identified
  12. 2017 Medium

    Established that both enzymatic domains are required in humans, via compound heterozygous mutations in each domain causing a multisystem ID phenotype.

    Evidence Clinical exome sequencing with domain mapping plus ndst1b morpholino knockdown in zebrafish

    PMID:28211985

    Open questions at the time
    • Recombinant activity of these specific variants not measured
    • Genotype-phenotype mapping limited to a single patient
  13. 2022 High

    Defined a dominant-negative splice variant (NDST1B) and demonstrated NDST1 self-association and assembly with EXT1/EXT2 by FRET.

    Evidence Recombinant NDST1B activity assays, HEK293 HS structural analysis, and FRET interaction mapping

    PMID:35137078

    Open questions at the time
    • Physiological abundance and regulation of NDST1B not established
    • Complex architecture remains uncharacterized at structural level
  14. 2023 High

    Dissected Wnt-pathway control, showing N-sulfation specifically drives Wnt8 cell-surface localization and signaling, and revealed an HS role in prion aggregate retention.

    Evidence Activity-specific NDST1 mutants with Wnt8 localization and TOP-Flash assays in Xenopus; neuronal Ndst1 knockout mice in prion infection with PET imaging

    PMID:36726238 PMID:37747931 PMID:38326088

    Open questions at the time
    • How N-sulfated HS spatially organizes Wnt ligands not structurally defined
    • Direct prion-HS binding kinetics not fully resolved
  15. 2024 High

    Proved that isolated loss of N-sulfotransferase activity is sufficient to cause human intellectual disability, cleanly separating the two catalytic functions in disease.

    Evidence Exome sequencing across families plus recombinant assay of p.(Gly611Ser) measuring both activities separately

    PMID:38129107

    Open questions at the time
    • Neuronal downstream signaling defect not directly mapped
    • Why N-sulfation loss specifically impairs cognition unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How NDST1 N-sulfated HS domains are spatially organized to selectively confer positive versus negative modulation of distinct morphogen pathways within a tissue remains unresolved.
  • No structural model of the NDST1-EXT GAGosome complex
  • Tissue-specific HS sequence-to-pathway rules not defined
  • Mechanism converting N-sulfation pattern into pathway selectivity unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 5 GO:0016787 hydrolase activity 3 GO:0140098 catalytic activity, acting on RNA 3
Localization
GO:0005794 Golgi apparatus 2
Pathway
R-HSA-1266738 Developmental Biology 6 R-HSA-162582 Signal Transduction 5 R-HSA-1430728 Metabolism 2
Partners
EXT1EXT2NDST1
Complex memberships
GAGosome (HS biosynthetic complex with EXT1/EXT2)

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 NDST1 is a bifunctional enzyme with separable N-deacetylase and N-sulfotransferase activities; active-site point mutations that selectively destroy N-deacetylase activity abolish HS N-sulfation entirely, demonstrating that N-deacetylation is prerequisite and rate-limiting for N-sulfation. Mutation of the N-sulfotransferase domain alone still produces oversulfated HS, and the data suggest two different enzyme molecules can act on the same glucosamine unit. Active-site mutagenesis of NDST1 cDNA; stable 293 cell lines expressing mutant enzymes; structural analysis of HS produced by transfected cells Biochemistry High 12590599
2002 NDST-1 and NDST-2 both N-deacetylate and N-sulfate heparan sulfate substrates; NDST-1 has an apparent Km of ~0.35 µM for heparan sulfate from human aorta, lower than for unsulfated K5 polysaccharide (~13.3 µM), indicating higher affinity for partially modified HS. Both isoforms are product-inhibited by N-sulfated sequences ≥6 sugar residues present in heparin and N-sulfated K5. Antibody-based N-deacetylase activity assay (JM-403 mAb recognizing N-unsubstituted glucosamine); conventional [3H]-acetate release assay; lysates of HEK293 cells stably transfected with NDST-1 or NDST-2 Glycobiology High 12634318
2004 Embryonic stem cells doubly deficient in NDST1 and NDST2 produce heparan sulfate that completely lacks N-sulfation yet still contains 6-O-sulfate groups, demonstrating that 6-O-sulfation can occur without prior N-sulfation and establishing the epistatic order of HS modification enzymes. NDST1/NDST2 double-knockout mouse ES cells; structural analysis of HS (disaccharide composition); RT-PCR for sulfotransferase expression The Journal of Biological Chemistry High 15319440
2004 Rat NDST-1 expressed in Saccharomyces cerevisiae as a soluble protein retains both N-deacetylase and N-sulfotransferase activities, requires Mn²⁺ for enzymatic activity, uses PAPS as sulfate donor, and can convert E. coli K5 polysaccharide to 60–65% N-sulfated heparosan. Yeast expression of recombinant NDST-1; heparin-Sepharose purification; enzymatic activity assays with defined substrates and cofactors Glycobiology High 15253930
2008 EXT2 overexpression enhances NDST1 protein levels, increases NDST1 N-glycosylation, and elevates HS sulfation, whereas EXT1 overexpression has opposite effects; co-immunoprecipitation indicated a direct interaction between EXT2 and NDST1, supporting incorporation of NDST1 into a GAGosome complex with the HS polymerase. Overexpression of EXT1/EXT2 in HEK293 cells; immunoprecipitation of EXT2–NDST1 complexes; NDST activity assay in transgenic mouse heart tissue; EXT1 gene-trap fibroblasts Proceedings of the National Academy of Sciences of the United States of America Medium 18337501
2000 Targeted disruption of NDST-1 in mice causes pulmonary hypoplasia, type II pneumocyte immaturity (increased glycogen, reduced lamellar bodies and microvilli), and reduced total phospholipids and disaturated phosphatidylcholine, establishing that NDST-1-dependent HS sulfation is required for type II pneumocyte maturation. Gene-targeted knockout mice (homologous recombination in ES cells); morphological and biochemical analysis of lung; lipid quantification FEBS Letters High 10664446
2005 Ndst1 loss-of-function in mice causes cerebral hypoplasia, absence of olfactory bulbs, eye defects, axon guidance errors, and craniofacial defects; the facial phenotype is consistent with impaired Sonic Hedgehog (Shh) and FGF signaling through mutant heparan sulfate, placing Ndst1 upstream of these morphogen pathways. Conditional Ndst1 knockout mice; phenotypic characterization; analysis of Shh and FGF signaling pathway activity Development (Cambridge, England) Medium 16020517
2006 Inactivation of Ndst1 in the lens reduces HS sulfation and diminishes binding of a subset of FGF proteins to FGF receptors, decreasing phospho-ERK and ERM expression, while BMP and Wnt signaling remain unchanged; this establishes Ndst1-dependent HS sulfation as specifically required for FGF signaling during lens development. Ndst1 conditional knockout mice; FGF–receptor binding assay; immunostaining for phospho-Erk and ERM; BMP/Wnt pathway reporter analysis Development (Cambridge, England) High 17107998
2007 Ndst1 deficiency in mice impairs FGF, Hedgehog, and Wnt signaling pathways and leads to neural tube fusion defects and skeletal abnormalities in addition to frontonasal dysplasia, establishing Ndst1 as a positive modulator of multiple HS-dependent growth factor/morphogen pathways during vertebrate development. Ndst1 knockout mice; in situ hybridization; analysis of FGF, Hedgehog, and Wnt signaling pathway components Developmental Dynamics Medium 17183530
2007 NDST-1 null mice show delayed endochondral bone formation; in situ HS-binding assay revealed decreased binding of BMP-2, -4, and -6 (but not FGF-1) to endogenous HS in mutant phalanges. Upregulation of BMPR-IA, phospho-Smad1, and PTHrP was observed, and blocking BMP signaling with noggin rescued chondrocyte hypertrophic differentiation defects, placing NDST-1-dependent HS as a negative modulator of BMP–PTHrP signaling in endochondral ossification. Ndst1 knockout mice; in situ HS binding assay with labeled growth factors; Western blot for signaling components; noggin rescue experiment in explant culture Bone High 17376755
2009 Loss of Ndst1 in mouse lung impairs BMP internalization by decreasing BMP binding to endogenous HS, leading to enhanced downstream BMP signaling in vivo; exogenous heparin rescues both BMP signaling and BMP internalization defects in Ndst1−/− lung, and noggin rescues Ndst1−/− lung morphogenetic defects in explant culture. Ndst1 knockout mice; BMP binding and internalization assays in lung cells; BMP signaling (pSmad) measurement; heparin rescue; noggin explant rescue Journal of Cell Science High 19299468
2010 Ndst1 deficiency in mammary epithelial cells reduces glucosamine N-sulfation and decreases FGF binding to mammary epithelial cells in vitro and in vivo, selectively blocking lobuloalveolar expansion without affecting ductal branching morphogenesis; lactational differentiation via STAT5 activation was unaffected, placing Ndst1 upstream of FGF-dependent lobuloalveolar development. Cre-loxP conditional Ndst1 knockout in mammary epithelium; FGF binding assay; STAT5 activation analysis; histology PLoS One High 20502530
2010 Smooth muscle-specific deletion of Ndst1 decreases N- and 2-O-sulfation of HS chains, reduces vascular smooth muscle cell (VSMC) proliferation, decreases femoral artery circumference, and significantly reduces lesion formation after vascular injury. Smooth muscle-specific Cre-loxP Ndst1 knockout mice; HS structural analysis; VSMC proliferation assay; vascular injury model Journal of Molecular and Cellular Cardiology Medium 20206635
2010 Ndst1-null mouse embryos lacking mandibular/TMJ structures show loss of Indian hedgehog (Ihh) signaling topography and ectopic ossification, establishing that Ndst1-dependent HS sulfation is required to restrict Ihh signaling to the appropriate zone in the condylar growth plate. Ndst1 knockout mice; in situ hybridization and immunostaining for Ihh pathway components; histological analysis Journal of Dental Research Medium 20554886
2013 miR-24 directly targets NDST1 to reduce HS sulfation and the binding affinity of HS for VEGFA; NDST1 suppression (by miR-24 or siRNA) also reduces VEGFR2 protein levels and blunts VEGFA-induced endothelial cell chemotaxis, establishing NDST1 as a downstream effector of miR-24 in modulating VEGFA signaling. miR-24 overexpression and siRNA knockdown of NDST1 in endothelial cells; HS sulfation measurement; VEGFA binding assay; VEGFR2 Western blot; chemotaxis assay The Journal of Biological Chemistry Medium 23884416
2013 Podocyte-specific deletion of Ndst1 causes foot process effacement and abnormal podocyte adhesion to Bowman's capsule without affecting agrin or perlecan core protein expression, demonstrating that HS N-sulfation is specifically required for podocyte organization. Podocyte-specific Ndst1 conditional knockout mice; electron microscopy; immunostaining; proteoglycan core protein expression analysis Kidney International Medium 23924956
2014 All four NDST1 missense mutations identified in autosomal recessive intellectual disability patients affect conserved residues in the sulfotransferase domain; Drosophila knockdown of sulfateless (NDST1 ortholog) impairs long-term memory, placing NDST1 N-sulfotransferase activity in a pathway required for cognition. Human exome/mutation analysis; mutation structural modeling; Drosophila sulfateless RNAi knockdown with long-term memory behavioral assay American Journal of Medical Genetics Part A Medium 25125150
2017 Compound heterozygous NDST1 mutations (one in the N-deacetylase domain, one in the sulfotransferase domain) cause intellectual disability with cranial nerve dysfunction, ataxia, and respiratory problems in a human patient, establishing that both enzymatic domains are required for normal NDST1 function in human development. Clinical exome sequencing; domain mapping of mutations; ndst1b morpholino knockdown in zebrafish causing craniofacial and developmental defects American Journal of Medical Genetics Part A Medium 28211985
2018 Conditional endothelial/myeloid Ndst1 deficiency in donor kidneys reduces HS sulfation, decreases CXC chemokine–HS interactions and NFκB/JAK-STAT pathway gene expression, and significantly reduces acute allograft rejection, establishing Ndst1-dependent HS sulfation as a driver of chemokine-mediated graft inflammation. Conditional Ndst1 knockout renal allografts transplanted into wildtype recipients; HS/CS disaccharide analysis; immunostaining; gene expression analysis; comparison to M-T7 chemokine-GAG inhibitor Scientific Reports Medium 30194334
2022 A splice variant of NDST1 (NDST1B, 825 aa) lacks both N-deacetylase and N-sulfotransferase activities. NDST1B overexpression reduces HS sulfation in HEK293 cells and acts in a dominant-negative manner, likely by replacing active NDST1 in biosynthetic enzyme complexes; FRET microscopy demonstrated that both NDST1A and NDST1B interact with EXT1, EXT2, and each other. Recombinant purified NDST1B enzymatic activity assay; HEK293 overexpression with HS structural analysis; FRET microscopy for protein–protein interactions; NDST enzyme activity measurement in lysates Glycobiology High 35137078
2023 Neuronal-specific depletion of Ndst1 in mice reduces HS sulfation on prion-bound HS chains (which are normally highly sulfated), prolongs survival in plaque-forming prion strains, reduces parenchymal plaque size, shortens fibrils, and accelerates clearance of extracellular prion protein monomers into CSF, demonstrating that Ndst1-dependent HS N-sulfation facilitates fibrillar prion aggregate retention in the brain parenchyma. Conditional neuronal/astrocyte Ndst1 knockout mice; prion infection survival analysis; plaque/fibril characterization; live PET imaging of recombinant PrP clearance; in vitro prion conversion assay PLoS Pathogens High 37747931
2023 Ndst1 in Xenopus activates Wnt signaling during neuroectodermal patterning; overexpression expands neural crest territory while morpholino-mediated knockdown reduces neural crest and trigeminal regions and causes cranial ganglion defects, placing Ndst1-modified HS upstream of Wnt pathway activation. Xenopus gain-of-function (overexpression) and loss-of-function (morpholino knockdown); in situ hybridization for neural crest and trigeminal markers; Wnt signaling reporter Development, Growth & Differentiation Medium 36726238
2024 The NDST1 missense variant p.(Gly611Ser), found in multiple intellectual disability families, results in complete loss of N-sulfotransferase activity while retaining N-deacetylase activity, demonstrating that isolated loss of the N-sulfotransferase function of NDST1 is sufficient to cause cognitive impairment. Exome sequencing in human families; recombinant wild-type and mutant NDST1 enzymatic activity assays (N-deacetylase and N-sulfotransferase activities measured separately) Human Molecular Genetics High 38129107
2024 In Xenopus embryos, N-sulfation (but not N-deacetylation) by NDST1 is responsible for Wnt8 localization on the cell surface and Wnt8 signaling; an NDST1 mutant with increased N-deacetylase but no N-sulfotransferase activity failed to increase Wnt8 cell-surface accumulation and reduced canonical Wnt signaling (TOP-Flash assay), while wild-type NDST1 overexpression increased both. NDST1 N-sulfotransferase-deficient mutant overexpression in Xenopus embryos; Wnt8 cell-surface localization assay; TOP-Flash canonical Wnt reporter assay; comparison to wild-type NDST1 Development, Growth & Differentiation High 38326088
2025 In Xenopus neural plate, NDST1-modified (N-sulfated) HS chains are dynamically polarized in a planar cell polarity (PCP)-dependent manner and co-polarize with Wnt11 and core PCP components; ndst1 knockdown disrupts Wnt11 localization and PCP formation, placing NDST1-dependent HS N-sulfation as required for Wnt11-mediated PCP. Ndst1 morpholino knockdown in Xenopus; antibody staining for polarized HS domains; live imaging of PCP components; Wnt11 localization assay bioRxivpreprint Medium

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Cerebral hypoplasia and craniofacial defects in mice lacking heparan sulfate Ndst1 gene function. Development (Cambridge, England) 161 16020517
2008 Heparan sulfate biosynthesis enzymes EXT1 and EXT2 affect NDST1 expression and heparan sulfate sulfation. Proceedings of the National Academy of Sciences of the United States of America 138 18337501
2000 Targeted disruption of NDST-1 gene leads to pulmonary hypoplasia and neonatal respiratory distress in mice. FEBS letters 131 10664446
2006 Heparan sulfate biosynthetic gene Ndst1 is required for FGF signaling in early lens development. Development (Cambridge, England) 90 17107998
2004 Heparan sulfate synthesized by mouse embryonic stem cells deficient in NDST1 and NDST2 is 6-O-sulfated but contains no N-sulfate groups. The Journal of biological chemistry 76 15319440
2002 Antibody-based assay for N-deacetylase activity of heparan sulfate/heparin N-deacetylase/N-sulfotransferase (NDST): novel characteristics of NDST-1 and -2. Glycobiology 69 12634318
2007 Heparan sulfate Ndst1 gene function variably regulates multiple signaling pathways during mouse development. Developmental dynamics : an official publication of the American Association of Anatomists 52 17183530
2014 NDST1 missense mutations in autosomal recessive intellectual disability. American journal of medical genetics. Part A 37 25125150
2009 NDST1-dependent heparan sulfate regulates BMP signaling and internalization in lung development. Journal of cell science 36 19299468
2010 Loss of the heparan sulfate sulfotransferase, Ndst1, in mammary epithelial cells selectively blocks lobuloalveolar development in mice. PloS one 34 20502530
2010 Sulfotransferase Ndst1 is needed for mandibular and TMJ development. Journal of dental research 31 20554886
2010 Heparan sulfate Ndst1 regulates vascular smooth muscle cell proliferation, vessel size and vascular remodeling. Journal of molecular and cellular cardiology 26 20206635
2003 Distinct effects on heparan sulfate structure by different active site mutations in NDST-1. Biochemistry 24 12590599
2013 MicroRNA-24 suppression of N-deacetylase/N-sulfotransferase-1 (NDST1) reduces endothelial cell responsiveness to vascular endothelial growth factor A (VEGFA). The Journal of biological chemistry 21 23884416
2013 Podocyte-specific deletion of NDST1, a key enzyme in the sulfation of heparan sulfate glycosaminoglycans, leads to abnormalities in podocyte organization in vivo. Kidney international 21 23924956
2004 Production of N-sulfated polysaccharides using yeast-expressed N-deacetylase/N-sulfotransferase-1 (NDST-1). Glycobiology 21 15253930
2007 NDST-1 modulates BMPR and PTHrP signaling during endochondral bone formation in a gene knockout model. Bone 19 17376755
2018 Selective Deletion of Heparan Sulfotransferase Enzyme, Ndst1, in Donor Endothelial and Myeloid Precursor Cells Significantly Decreases Acute Allograft Rejection. Scientific reports 18 30194334
2015 Direct interaction of Ste11 and Mkk1/2 through Nst1 integrates high-osmolarity glycerol and pheromone pathways to the cell wall integrity MAPK pathway. FEBS letters 16 26787465
2019 Integrative Analysis Identified IRF6 and NDST1 as Potential Causal Genes for Ischemic Stroke. Frontiers in neurology 15 31156544
2022 A natural mutation of the NST1 gene arrests secondary cell wall biosynthesis in the seed coat of a hull-less pumpkin accession. Horticulture research 14 36072840
2019 MiRNA-191 functions as an oncogene in primary glioblastoma by directly targeting NDST1. European review for medical and pharmacological sciences 14 31364126
2017 A girl with developmental delay, ataxia, cranial nerve palsies, severe respiratory problems in infancy-Expanding NDST1 syndrome. American journal of medical genetics. Part A 14 28211985
2004 Altered expression of NDST-1 messenger RNA in puromycin aminonucleoside nephrosis. The Journal of laboratory and clinical medicine 9 14966466
2022 A dominant negative splice variant of the heparan sulfate biosynthesis enzyme NDST1 reduces heparan sulfate sulfation. Glycobiology 8 35137078
2016 NDST1 Preferred Promoter Confirmation and Identification of Corresponding Transcriptional Inhibitors as Substrate Reduction Agents for Multiple Mucopolysaccharidosis Disorders. PloS one 6 27657498
2012 Smooth muscle specific deletion of Ndst1 leads to decreased vessel luminal area and no change in blood pressure in conscious mice. Journal of cardiovascular translational research 6 22555965
2023 Alternative Splicing for Leucanthemella linearis NST1 Contributes to Variable Abiotic Stress Resistance in Transgenic Tobacco. Genes 4 37628601
2021 Yeast Nst1 is a novel component of P-bodies and is a specific suppressor of proteasome base assembly defects. Molecular biology of the cell 4 34347506
2024 Loss of NDST1 N-sulfotransferase activity is associated with autosomal recessive intellectual disability. Human molecular genetics 3 38129107
2023 Ndst1, a heparan sulfate modification enzyme, regulates neuroectodermal patterning by enhancing Wnt signaling in Xenopus. Development, growth & differentiation 3 36726238
2022 Nst1, Densely Associated to P-Body in the Post-Exponential Phases of Saccharomyces cerevisiae, Shows an Intrinsic Potential of Producing Liquid-Like Condensates of P-Body Components in Cells. International journal of molecular sciences 3 35269643
2022 The Multivalent Polyampholyte Domain of Nst1, a P-Body-Associated Saccharomyces cerevisiae Protein, Provides a Platform for Interacting with P-Body Components. International journal of molecular sciences 3 35806385
2013 Vascular biomechanical properties in mice with smooth muscle specific deletion of Ndst1. Molecular and cellular biochemistry 3 24101444
2024 Dissection of N-deacetylase and N-sulfotransferase activities of NDST1 and their effects on Wnt8 distribution and signaling in Xenopus embryos. Development, growth & differentiation 2 38326088
2023 Neuronal Ndst1 depletion accelerates prion protein clearance and slows neurodegeneration in prion infection. PLoS pathogens 2 37747931
2022 Overexpression of NDST1 Attenuates Fibrotic Response in Murine Adipose-Derived Stem Cells. Stem cells and development 1 35920108
2022 The role and mechanism of NDST1/NULP1 regulating right ventricular hypertrophy in hypoxic pulmonary hypertension. General physiology and biophysics 1 36222339

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