Results 161 to 170 of about 15,873 (215)

The sulfatase gene family

open access: yesCurrent Opinion in Genetics and Development, 1997
During the past few years, molecular analyses have provided important insights into the biochemistry and genetics of the sulfatase family of enzymes, identifying the molecular bases of inherited diseases caused by sulfatase deficiencies.
Giancarlo Parenti   +2 more
exaly   +8 more sources

Activatable Near-Infrared Fluorescent and Photoacoustic Dual-Modal Probe for Highly Sensitive Imaging of Sulfatase In Vivo

open access: yesACS Sensors, 2023
Sulfatase is an important biomarker closely associated with various diseases. However, the state-of-the-art sulfatase probes are plagued with a short absorption/emission wavelength and limited sensitivity.
Lian Xia, Fengli Qu, Mei-Hao Xiang
exaly   +2 more sources

Steroid Sulfatase Deficiency [PDF]

open access: yesPediatric Research, 1977
Placental steroid sulfatase deficiency is a genetic disorder only recently reported in the medical literature. Most documented cases of placental sulfatase deficiency have been marked by delay in onset of labor, lack of cervical dilatation, and relative refractoriness of oxytocic agents and amniotomy. We have studied the placenta, cultured fibroblasts,
Richard L Stevens   +2 more
exaly   +3 more sources
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Steroid sulfatase, arylsulfatases A and B, galactose-6-sulfatase, and iduronate sulfatase in mammary cells and effects of sulfated and non-sulfated estrogens on sulfatase activity

Journal of Steroid Biochemistry and Molecular Biology, 2007
Sulfatase enzymes have important roles in metabolism of steroid hormones and of glycosaminoglycans (GAGs). The activity of five sulfatase enzymes, including steroid sulfatase (STS; arylsulfatase C), arylsulfatase A (ASA; cerebroside sulfatase), arylsulfatase B (ASB; N-acetylgalactosamine-4-sulfatase), galactose-6-sulfatase (GALNS), and iduronate-2 ...
Joanne K Tobacman, Sumit Bhattacharyya
exaly   +3 more sources

Steroid sulfatase inhibitors

Expert Opinion on Therapeutic Patents, 2003
AbstractSteroid sulfatase (STS) regulates the local production of estrogens and androgens from systemic precursors in several tissues. The enzyme catalyzes the hydrolysis of the sulfate esters of 3‐hydroxy steroids, which are inactive transport or precursor forms of the active 3‐hydroxy steroids.
Peter, Nussbaumer, Andreas, Billich
openaire   +2 more sources

Structure of a human lysosomal sulfatase

open access: yesStructure, 1997
Background: Sulfatases catalyze the hydrolysis of sulfuric acid esters from a wide variety of substrates including glycosaminoglycans, glycolipids and steroids.
Charles S Bond   +2 more
exaly   +2 more sources

Rapid degradation of steroid sulfatase in multiple sulfatase deficiency

Biochemical and Biophysical Research Communications, 1986
Pulse labeling followed by SDS-PAGE electrophoresis of immunoprecipitated [35S]methionine-labeled steroid sulfatase (STS) gave a single band of molecular weight 65,000 daltons. After a chase period of 18 hours the material appeared as molecular weight approximately 64,000.
A L, Horwitz   +3 more
openaire   +2 more sources

Lysosomal sulfatases: a growing family

Biochemical Journal, 2020
Sulfatases constitute a family of enzymes that specifically act in the hydrolytic degradation of sulfated metabolites by removing sulfate monoesters from various substrates, particularly glycolipids and glycosaminoglycans. A common essential feature of all known eukaryotic sulfatases is the posttranslational modification of a critical cysteine residue ...
Lübke, Torben, Damme, Markus
openaire   +2 more sources

SULFATASES AND HUMAN DISEASE

Annual Review of Genomics and Human Genetics, 2005
▪ Abstract  Sulfatases are a highly conserved family of proteins that cleave sulfate esters from a wide range of substrates. The importance of sulfatases in human metabolism is underscored by the presence of at least eight human monogenic diseases caused by the deficiency of individual sulfatases. Sulfatase activity requires a unique posttranslational
DIEZ ROUX G., BALLABIO, ANDREA
openaire   +3 more sources

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