ArticleThe Journal of biological chemistry2014
Molecular characterization of arylsulfatase G: expression, processing, glycosylation, transport, and activity.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Programmed-Cell-Death-Related Signature Reveals Immune Microenvironment Characteristics and Predicts Therapeutic Response in Diffuse Large B Cell Lymphoma.Biomedicines · 2025Article
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- TMEM106B deficiency leads to alterations in lipid metabolism and obesity in the TDP-43Communications biology · 2025Article
- Mucopolysaccharidosis Type IIIE: A Real Human Disease or a Diagnostic Pitfall?Diagnostics (Basel, Switzerland) · 2024Review
- Usher syndrome type IV: clinically and molecularly confirmed by novel ARSG variants.Human genetics · 2022Article
- Novel subtype of mucopolysaccharidosis caused by arylsulfatase K (ARSK) deficiency.Journal of medical genetics · 2022Article
- Sperm DNA methylation patterns at discrete CpGs and genes involved in embryonic development are related to bull fertility.BMC genomics · 2022Article
- Development of novel monoclonal antibodies and immunoassays for sensitive and specific detection of SULF1 endosulfatase.Biochimica et biophysica acta. General subjects · 2021Article
- A Possible Role for Arylsulfatase G in Dermatan Sulfate Metabolism.International journal of molecular sciences · 2020Article
- Differential gene expression during substrate probing in larvae of the Caribbean coral Porites astreoides.Molecular ecology · 2019Article
- A homozygous founder missense variant in arylsulfatase G abolishes its enzymatic activity causing atypical Usher syndrome in humans.Genetics in medicine : official journal of the American College of Medical Genetics · 2018Article
- Canine neuronal ceroid lipofuscinoses: Promising models for preclinical testing of therapeutic interventions.Neurobiology of disease · 2017Review
- Disruption of the vacuolar-type HAutophagy · 2017Article
- Quantitative Proteome Analysis of Mouse Liver Lysosomes Provides Evidence for Mannose 6-phosphate-independent Targeting Mechanisms of Acid Hydrolases in Mucolipidosis II.Molecular & cellular proteomics : MCP · 2017Article
- Arylsulfatase K is the Lysosomal 2-Sulfoglucuronate Sulfatase.ACS chemical biology · 2017Article
- Subcellular Trafficking of Mammalian Lysosomal Proteins: An Extended View.International journal of molecular sciences · 2016Review
- Sanfilippo syndrome: causes, consequences, and treatments.The application of clinical genetics · 2015Review
- Profiling of concanavalin A-binding glycoproteins in human hepatic stellate cells activated with transforming growth factor-β1.Molecules (Basel, Switzerland) · 2014Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arylsulfatase G (ARSG) is a recently identified lysosomal sulfatase that was shown to be responsible for the degradation of 3-O-sulfated N-sulfoglucosamine residues of heparan sulfate glycosaminoglycans. Deficiency of ARSG leads to a new type of mucopolysaccharidosis, as described in a mouse model. Here, we provide a detailed molecular characterization of the endogenous murine enzyme. ARSG is expressed and proteolytically processed in a tissue-specific manner. The 63-kDa single-chain precursor protein localizes to pre-lysosomal compartments and tightly associates with organelle membranes, most likely the endoplasmic reticulum. In contrast, proteolytically processed ARSG fragments of 34-, 18-, and 10-kDa were found in lysosomal fractions and lost their membrane association. The processing sites and a disulfide bridge between the 18- and 10-kDa chains could be roughly mapped. Proteases participating in the processing were identified as cathepsins B and L. Proteolytic processing is dispensable for hydrolytic sulfatase activity in vitro. Lysosomal transport of ARSG in the liver is independent of mannose 6-phosphate, sortilin, and Limp2. However, mutation of glycosylation site N-497 abrogates transport of ARSG to lysosomes in human fibrosarcoma cells, due to impaired mannose 6-phosphate modification.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.