Disease relevance of Chst11

• Mouse mastocytoma cells grown in suspension culture produce chondroitin 4-sulphate [1].
• Digestion with chondroitinase AC, ABC and streptomyces hyaluronidase suggested significant differences between control and diabetic bone matrix in the levels of chondroitin 4 and 6 sulfates (p less than 0.05) and hyaluronic acid (p less than 0.001) but not dermatan sulfate [2].

High impact information on Chst11

• Saturation of the heparan sulfate binding sites on the collagen substrata with heparan sulfate or heparin, prior to cell inoculation, abolished the ability to support cell adhesion, whereas chondroitin 4 sulfate, chondroitin 6 sulfate, and hyaluronic acid had no effect [3].
• Maintenance of chondroitin sulfation balance by chondroitin-4-sulfotransferase 1 is required for chondrocyte development and growth factor signaling during cartilage morphogenesis [4].
• Extracellular matrix (ECM) molecules, including chondroitin-4 or chondroitin-6 sulfate proteoglycans (CSPGs) and tenascin, are upregulated in and around wounds and transplants to the adult CNS [5].
• To elucidate the distribution of such functional sugar chains during the development of the brain, in situ hybridization was performed to examine expression of three CS/DS GalNAc 4-O-sulfotransferases, D4ST-1, C4ST-1, and C4ST-2, and a single uronyl 2-O-sulfotransferase (UST) involved in the biosynthesis of DS in addition to CS intermediates [6].
• The chondroitin sulfate chains contained exclusively chondroitin 4- and 6-sulfate; however, the ratio of these two disaccharides differed between the medium- and cell-associated proteoglycans, and changed during progression of the cells into a fully differentiated phenotype [7].

Biological context of Chst11

• One of the genes encodes for Chondroitin-4-sulfotransferase and displays a highly specific temporal and spatial expression pattern during mouse embryogenesis [8].
• The purified enzyme catalyzed the hydrolysis of p-nitrocatechol sulfate (pNCS), 4-methylumbelliferyl sulfate (4MUS), and chondroitin-4-sulfate (C4S) heptasaccharide [9].

Anatomical context of Chst11

• These results show that chondroitin 4-O-sulfation by C4st1 is required for proper chondroitin sulfate localization, modulation of distinct signaling pathways and cartilage growth plate morphogenesis [4].
• Whereas FDCP-Mix A4 cells synthesize a homogeneous chondroitin 4-sulphate proteoglycan, isolation and characterization of proteoglycans from the human cell line TF-1 revealed, that TF-1 cells synthesize, in addition to a chondroitin sulphate proteoglycan, a heparan sulphate proteoglycan as major proteoglycan [10].
• AKTB-1b follows the pattern of normal B cells, whilst in EL-4 only chondroitin 4-sulphate is synthesized [11].
• Chondroitin sulfates in developing mouse tooth germs. An immunohistochemical study with monoclonal antibodies against chondroitin-4 and chondroitin-6 sulfates [12].
• Chondroitin 4- and chondroitin 6-sulfates were present in the stellate reticulum but otherwise they were confined to the dental mesenchyme [12].

Associations of Chst11 with chemical compounds

• To compare the hemolytic efficiencies of C4s and C4p, a solid-phase competitive radioimmunoassay was developed to permit measurement of the small quantities of C4 antigen in these cultures [13].
• Heparan sulfate, keratan sulfate, chondroitin, chondroitin 4/6-sulfate (80% 4-sulfate and 20% 6-sulfate), and UDP-N-acetylgalactosamine 4-sulfate were used as acceptors for the measurement of 3'-phosphoadenylyl sulfate: glycosaminoglycan sulfotransferase activities in human serum [14].
• Thus hyaluronic acid, dermatan sulphate, chondroitin-4-sulphate, chondroitin-6-sulphate, and even unchanged dextran all potentiated aFGF induced neuronal survival [15].
• Inhibition studies showed that chondroitin 6-sulfate inhibited the bacteriolytic activity of lysozyme in a competitive manner more efficiently than heparin and chondroitin 4-sulphate [16].
• The substrates included native bovine dermal collagen, succinylated, acetylated and methylated collagen, and a series of composite materials formed from collagen and the glycosaminoglycans hyaluronic acid, chondroitin 4-sulphate and chondroitin 6-sulphate and the glycoprotein fibronectin [17].

Other interactions of Chst11

• Chondroitin-4-sulphate (proteoglycan), a receptor for Plasmodium falciparum-infected erythrocyte adherence on brain microvascular endothelial cells [18].

Analytical, diagnostic and therapeutic context of Chst11

• Consistent with results published previously staining with haematoxylin-eosin or Alcian blue, immunohistochemical analysis, and quantitative RT-PCR confirmed the expression of chondrogenic markers (chondroitin-4- and -6-sulfate as well as type II collagen) [19].
• Immunostaining with the monoclonal antibody 5-D-4 before and after treatment with chondroitin-4- and chondroitin-6-sulfatase confirmed the presence of keratan sulfate (KS), a sialylated proteoglycan, in dentinal tubules [20].
• The induced glycosaminoglycan depletion in the extracellular matrix was monitored by immunohistochemistry employing monoclonal antibodies to chondroitin 4- and chondroitin 6-sulfates. beta-Xyloside inhibited formation of the dental bell and delayed the appearance of the first odontoblasts [21].

References