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Sulfatase 1

Heparan sulfate proteoglycans (HSPGs) act as coreceptors for numerous heparin-binding growth factors and cytokines and are involved in cell signaling. Heparan sulfate 6-O-endosulfatases, such as SULF1, selectively remove 6-O-sulfate groups from heparan sulfate. This activity modulates the effects of heparan sulfate by altering binding sites for signaling molecules (Dai et al., 2005 [PubMed 16192265]).[supplied by OMIM, Mar 2008] (from NCBI)
Top mentioned proteins: CAN, HAD, IDS, aromatase, AGE
Papers on sulfatase
Estrone sulfate and dehydroepiandrosterone sulfate: Transactivation of the estrogen and androgen receptor.
Bonefeld-Jørgensen et al., Århus, Denmark. In Steroids, Jan 2016
The enzyme steroid sulfatase (STS) cleaves the sulfate group of DHEAS and E1S leading to biosynthesis of endogenous hormones such as testosterone and estrone.
Effects of steroid hormone on estrogen sulfotransferase and on steroid sulfatase expression in endometriosis tissue and stromal cells.
Ferriani et al., São Paulo, Brazil. In J Steroid Biochem Mol Biol, Jan 2016
The potential roles of female steroid hormones in modulating key estrogen-metabolizing enzymes, steroid sulfatase (STS) and estrogen sulfotransferase (SULT1E1), were investigated.
X‑linked ichthyosis and Crigler‑Najjar syndrome Ⅰ: Coexistence in a male patient with two copy number variable regions of 2q37.1 and Xp22.3.
Song et al., Beijing, China. In Mol Med Report, Jan 2016
UNASSIGNED: X‑linked ichthyosis (XLI) is an X‑linked recessive skin disorder generally restricted to males, which arises from mutations in the steroid sulfatase (STS) gene located on Xp22.3.
Bone mineral density in MPS IV A (Morquio syndrome type A).
Tomatsu et al., Wilmington, United States. In Mol Genet Metab, Jan 2016
UNASSIGNED: Mucopolysaccharidosis IV A (MPS IV A), Morquio A, is caused by deficiency in lysosomal enzyme N-acetylgalactosamine-6-sulfate sulfatase (GALNS), which is responsible for the catabolism of the glycosaminoglycans (GAGs) keratan sulfate (KS) and chondroitin 6-sulfate (C6S).
Pharmacodynamics, pharmacokinetics and biodistribution of recombinant human N-acetylgalactosamine 4-sulfatase after 6months of therapy in cats using different IV infusion durations.
O'Neill et al., Philadelphia, United States. In Mol Genet Metab, Nov 2015
BACKGROUND: Mucopolysaccharidosis VI (MPS VI) is a lysosomal storage disease characterized by an absence or marked reduction of lysosomal N-acetylgalactosamine-4-sulfatase activity.
Estrogen O-sulfamates and their analogues: Clinical steroid sulfatase inhibitors with broad potential.
Potter et al., Bath, United Kingdom. In J Steroid Biochem Mol Biol, Sep 2015
Estrogen sulfamate derivatives were the first irreversible active-site-directed inhibitors of steroid sulfatase (STS), an emerging drug target for endocrine therapy of hormone dependent diseases that catalyzes inter alia the hydrolysis of estrone sulfate to estrone.
Breast cancer treatment and sulfotransferase.
Cho et al., Beijing, China. In Expert Opin Ther Targets, Jun 2015
EXPERT OPINION: The prevention of estrogen binding to ER by antiestrogen and inhibition of estrogen synthesis by aromatase or sulfatase inhibitor have been used in clinical therapy for breast cancer.
Impact of enzyme replacement therapy and hematopoietic stem cell transplantation in patients with Morquio A syndrome.
Orii et al., Wilmington, United States. In Drug Des Devel Ther, 2014
Recombinant N-acetylgalactosamine-6-sulfate sulfatase (GALNS) in Escherichia coli BL21 (DE3) (erGALNS) and in the methylotrophic yeast Pichia pastoris (prGALNS) has been produced as an alternative to the conventional production in Chinese hamster ovary cells.
Cytogenetic analysis of epithelial ovarian cancer's stem cells: an overview on new diagnostic and therapeutic perspectives.
Triolo et al., In Eur J Gynaecol Oncol, 2014
The progression of EOC is characterized by a series of combined epigenetic aberrations, including the most important of those determined by the loss of methylation of certain regions of DNA encoding genes such as Ras-association domain-containing family 1 [(RASSF1A) tumor suppressor], death-associated protein kinase [(DAPK) protein kinase associated with the regulation of apoptosis], human sulfa- tase-I [(hSulf-1) sulfatase, which plays a key role in the regulation of apoptosis], breast cancer 1 gene [(BRCA1) tumor suppressor gene, involved in the processes of DNA repair], and HOXAI0 (gene required to promote many transcription factors).
Neonatal multiple sulfatase deficiency with a novel mutation and review of the literature.
Dursun et al., Antalya, Turkey. In Turk J Pediatr, 2014
Multiple sulfatase deficiency is a rare autosomal recessive disorder in which affected individuals present a complex phenotype due to the impaired activity of all sulfatases.
A developmental switch coupled to the evolution of plasticity acts through a sulfatase.
Sommer et al., Tübingen, Germany. In Cell, 2013
EUD-1 is a sulfatase that acts dosage dependently, is necessary and sufficient to control the sexual dimorphism of feeding forms, and has a conserved function in Pristionchus evolution.
Up-regulated expression of sulfatases (SULF1 and SULF2) as prognostic and metastasis predictive markers in human gastric cancer.
Yang et al., Seoul, South Korea. In J Pathol, 2012
SULF1 may serve as a promising biomarker for patients with gastric carcinoma.
Organ-specific sulfation patterns of heparan sulfate generated by extracellular sulfatases Sulf1 and Sulf2 in mice.
Keino-Masu et al., Tsukuba, Japan. In J Biol Chem, 2012
Sulf1 and Sulf2 differentially contribute to the generation of organ-specific sulfation patterns of heparan sulfate.
Endo-sulfatase Sulf-1 protein expression is down-regulated in gastric cancer.
Rajkumar et al., Chennai, India. In Asian Pac J Cancer Prev, 2011
Sulf-1 protein expression is down-regulated in gastric cancer.
HSulf-1 inhibits cell proliferation and invasion in human gastric cancer.
Zhou et al., Beijing, China. In Cancer Sci, 2011
extracellular HSulf-1 may function as a negative regulator of proliferation and invasion in gastric cancer by suppressing Wnt/beta-catenin signaling at the cell surface.
SULFs in human neoplasia: implication as progression and prognosis factors.
Klein et al., Montpellier, France. In J Transl Med, 2010
SULF1 and SULF2 are overexpressed in various human cancer types and can be associated to progression and prognosis.
Molecular basis for multiple sulfatase deficiency and mechanism for formylglycine generation of the human formylglycine-generating enzyme.
Rudolph et al., Göttingen, Germany. In Cell, 2005
Inactivity of FGE results in multiple sulfatase deficiency (MSD), a fatal autosomal recessive syndrome.
Steroid sulfatase: molecular biology, regulation, and inhibition.
Potter et al., London, United Kingdom. In Endocr Rev, 2005
Steroid sulfatase (STS) is responsible for the hydrolysis of aryl and alkyl steroid sulfates and therefore has a pivotal role in regulating the formation of biologically active steroids.
The multiple sulfatase deficiency gene encodes an essential and limiting factor for the activity of sulfatases.
Ballabio et al., Napoli, Italy. In Cell, 2003
In multiple sulfatase deficiency (MSD), a human inherited disorder, the activities of all sulfatases are impaired due to a defect in posttranslational modification.
Deficiencies of glucosamine-6-sulfate or galactosamine-6-sulfate sulfatases are responsible for different mucopolysaccharidoses.
Caskey et al., Houston, United States. In Science, 1978
[1-3H]Galactitol-6-sulfate, N- [1-3H]acetylgalactosaminitol-6-sulfate, N-[1-3H]acetylglucosaminitol-6-sulfate, N-acetylglucosamine-6-sulfate, and 6-sulfated tetrasaccharides from chondroitin-6-sulfate have been used for the measurement of 6-sulfatase activity of extracts of normal skin fibroblasts and of fibroblasts cultured from patients with genetic mucopolysaccharidoses.
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