dermatan sulfate
dermatan sulphate

This is due to an excess of dermatan sulfate, a glycosaminoglycan.

Dermatan sulfate accumulates abnormally in several of the mucopolysaccharidosis disorders.

This enzyme acts on chondroitin 4-sulfate, chondroitin 6-sulfate and dermatan sulfate.

It is a component of dermatan sulfate and heparan sulfate, which are glycosaminoglycans.

The accumulated substrate in Hunter's syndrome is heparan sulfate and dermatan sulfate.

It is involved in the degeneration of glycosaminoglycans such as dermatan sulfate and heparan sulfate.

Dermatan sulfate may have roles in coagulation, cardiovascular disease, carcinogenesis, infection, wound repair, and fibrosis.

This enzyme catalyses the hydrolysis of unsulfated alpha-L-iduronosidic linkages in dermatan sulfate.

Anterior to Bowman layer, deposits of glycosaminoglycan were detected and identified as chondroitin-4-sulfate and dermatan sulfate.

The first step in the breakdown of dermatan sulfate and heparan sulfate requires the lysosomal enzyme I2S.

The dermatan sulfate side chains of decorin aggregate in solution, and this behavior can assist with the assembly of the collagen fibrils.

Dermatan sulfate is a glycosaminoglycan (formerly called a mucopolysaccharide) found mostly in skin, but also in blood vessels, heart valves, tendons, and lungs.

Sulodexide is a highly purified mixture of glycosaminoglycans composed of low molecular weight heparin (80%) and dermatan sulfate (20%).

The degeneration occurs in conjunction with an accumulation of dermatan sulfate, a glycosaminoglycan, within the connective tissue matrix of the valve.

It consists of a mixture of heparan sulfate, dermatan sulfate, and chondroitin sulfate.

The ESM-1 gene product is also called endocan since 2001, when it was characterized as a dermatan sulfate proteoglycan by Bechard et al.

This test is performed to detect a rare disorder of excess acid mucopolysaccharides accumulation (especially dermatan sulfate and heparan sulfate) in the tissues.

In Hunter syndrome, the problem concerns the breakdown of two GAG: dermatan sulfate and heparan sulfate.

As a result, GAG build up in cells throughout the body, particularly in tissues that contain large amounts of dermatan sulfate and heparan sulfate.

The defective alpha-L-iduronidase results in an accumulation of heparan and dermatan sulfate within phagocytes, endothelium, smooth muscle cells, neurons, and fibroblasts.

ARSB targets two GAGs in particular: dermatan sulfate and chondroitin sulfate.

"Chondroitin sulfate B" is an old name for dermatan sulfate, and it is no longer classified as a form of chondroitin sulfate.

The syndrome is characterized by a deficiency in the enzyme arylsulfatase B (also called N- acetylgalactosamine-4-sulfatase), which leads to an excess of dermatan sulfate in the urine.

Carbohydrate sulfotransferase D4ST1, which transfers sulfate to position 4 of the GalNAc residue of dermatan sulfate.

Danaparoid, a mixture of heparan sulfate, dermatan sulfate, and chondroitin sulfate, can be used as an anticoagulant in patients that have developed HIT.