Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.6.4 (chondroitinase)
 2,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proteoglycans appear to play an important role in modulating cell-cell and cell-matrix interactions during nervous tissue histogenesis. The nervous tissue-specific chondroitin sulfate proteoglycans neurocan and phosphacan/protein-tyrosine phosphatase-zeta/beta were found to be high-affinity ligands of the neural cell adhesion molecule TAG-1/axonin-1, with dissociation constants of 0.3 nM and 0.04 nM, respectively. Phosphacan binding was decreased by approximately 70% following chondroitinase treatment, whereas binding of neurocan was not affected. The contribution of chondroitin sulfate chains to the binding of neurocan and phosphacan to TAG-1/axonin-1 is therefore the opposite of that previously observed for their binding to two other Ig-superfamily neural cell adhesion molecules, Ng-CAM/L1 and N-CAM. Moreover, whereas phosphacan interactions with certain proteins are mediated at least in part by N-linked oligosaccharides on the proteoglycan, N-deglycosylation of phosphacan had no effect on its binding to TAG-1/axonin-1. In addition to the chondroitin sulfate proteoglycans described above, we have demonstrated that N-CAM is a high-affinity ligand of TAG-1/axonin-1 (Kd approximately 1 nM), and specific binding of TAG-1/axonin-1 to tenascin-C was also observed (Kd approximately 9 nM). Immunocytochemical studies of embryonic and early postnatal nervous tissue showed an overlapping localization of TAG-1/axonin-1 with all four of these ligands, further supporting the biological significance of their ability to interact in vitro.
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PMID:TAG-1/axonin-1 is a high-affinity ligand of neurocan, phosphacan/protein-tyrosine phosphatase-zeta/beta, and N-CAM. 866 15

During the initial stages of development, the notochord provides repulsive signals for dorsal root ganglion (DRG) axons via semaphorin 3A/neuropilin-1, axonin-1/SC2, and other unknown repulsive molecules. The notochord is known to produce aggrecan, one of the chondroitin sulfate proteoglycans (CSPGs). We report here that adding aggrecan to the culture medium cannot only induce DRG growth cone collapse, but also inhibit DRG axonal growth. Using cocultures composed of tissues derived from chick embryos or neuropilin-1-deficient mice treated with chondroitinase ABC, we show the direct evidence that CSPGs are involved in notochord-derived repulsion for DRG axons. At later developmental stages, CSPGs are involved in perinotochordal sheath-derived axon repulsion, but not in notochord core-derived repulsion. We further demonstrate that TAG-1/axonin-1/SC2 is not involved in mediating repulsive activities by CSPGs, but is required for notochord core-derived axon repulsion. Thus, notochord-derived multiple axon repulsions act in a spatiotemporal-specific manner to shape the initial trajectories of DRG axons.
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PMID:Developmental regulation of notochord-derived repulsion for dorsal root ganglion axons. 1501 39

The hypothalamic magnocellular neurons, synthesizing arginine vasopressin (AVP) and oxytocin, are well known to show structural plasticity during chronic physiological stimulation. We have previously reported that 6B4 phosphacan/receptor-type protein-tyrosine phosphatasebeta (RPTPbeta), a chondroitin sulfate proteoglycan is highly expressed in the supraoptic nucleus (SON) of adult hypothalamus. Here, we undertook to study the activity-dependent regulation of 6B4 phosphacan/RPTPbeta in this system. Double labeling confocal microscopy demonstrated in the SON that 6B4 phosphacan/RPTPbeta-immunoreactive perineuronal nets were seen around AVP-containing somata and dendrites and its distribution pattern was well coincided with that of TAG-1. Quantitative immunohistochemical and Western analyses showed that 1-week salt loading, known as the chronic physiological stimulation for inducing the structural changes such as synaptic remodeling and direct neuronal membrane apposition, decreased 6B4 phosphacan/RPTPbeta levels in the SON, but did not alter TAG-1 levels. The 6B4 phosphacan/RPTPbeta levels were returned to control basal values within 3 weeks after the cessation of the chronic stimulation. Activity-dependent decreases in 6B4 phosphacan/RPTPbeta levels of the SON were confirmed when Western and immunohistochemical samples were digested with chondroitinase ABC, indicating that the decrease in 6B4 phosphacan/RPTPbeta levels was due to disappearance of 6B4 phosphacan/RPTPbeta core protein rather than increase in chondroitin sulfate glycosaminoglycans. With electron microscopy, the electron-dense immunoproducts for 6B4 phosphacan/RPTPbeta were found on the membrane surface of axons and glial processes, but not at synaptic junctions in control SON, and its immunoreactivity was eliminated with the chronic salt loading. The present results indicate that the levels of 6B4 phosphacan/RPTPbeta are regulated with activity-dependent manner and may be concerned with the structural plasticity seen in the SON.
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PMID:Activity-dependent regulation of a chondroitin sulfate proteoglycan 6B4 phosphacan/RPTPbeta in the hypothalamic supraoptic nucleus. 1526 Nov 12