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1 r CSPG core proteins, including aggrecan and neurocan.
2 oteoglycans, such as versican, brevican, and neurocan.
3 ondroitin sulfate proteoglycans brevican and neurocan.
4 the re-expression of the neonatal isoform of neurocan.
5 l but significant decrease in the binding of neurocan.
6 , and heightened expression of CSPGs such as neurocan and aggrecan that may inhibit remyelination.
7 paran sulphate-PGs and 2.2-fold reduction in neurocan and brevican core proteins in scar tissue.
8 tify two other aggrecan gene family members, neurocan and brevican, in the adult spinal cord.
9  decreased levels of the inhibitory proteins neurocan and CD44 within the retina.
10 ated levels of the inhibitory ECM molecules (neurocan and CD44) remained.
11                                  However, L1-neurocan and L1-neuropilin binding were preserved and se
12 hat TBI resulted in an increase in the CSPGs neurocan and NG2 expression in a tight band surrounding
13 -specific chondroitin sulfate proteoglycans, neurocan and phosphacan (the extracellular domain of pro
14            The chondroitin sulfate chains on neurocan and phosphacan account for at least 80% of thei
15                                              Neurocan and phosphacan are also high affinity ligands o
16                                  Conversely, Neurocan and Phosphacan broadly decrease with time in al
17                                              Neurocan and phosphacan can be localized to reactive ast
18 recan presented a biphasic expression, while Neurocan and Phosphacan expression declined dramatically
19 l results demonstrate that the expression of neurocan and phosphacan follow different developmental t
20 mistry, we have compared the distribution of neurocan and phosphacan in the developing central nervou
21           By E16-19, strong staining of both neurocan and phosphacan is seen in the marginal zone and
22 chondroitin sulfate chains to the binding of neurocan and phosphacan to TAG-1/axonin-1 is therefore t
23 e-specific chondroitin sulfate proteoglycans neurocan and phosphacan with the extracellular matrix pr
24  revealed differences in the interactions of neurocan and phosphacan with the two major members of th
25 s of two major nervous tissue proteoglycans, neurocan and phosphacan, in embryonic and postnatal rat
26 e-specific chondroitin sulfate proteoglycans neurocan and phosphacan/protein-tyrosine phosphatase-zet
27                                    Brevican, neurocan and versican however, did not accumulate at all
28  proteoglycans including aggrecan, versican, neurocan, and brevican.
29 rate upregulation of versican, brevican, and neurocan, and downregulation of phosphacan.
30                                    Weak ED1, neurocan, and NG2-positive signal was detected 4 weeks p
31  chondroitin sulfate proteoglycans aggrecan, neurocan, and versican are expressed by cells in both th
32 teoglycans that includes aggrecan, brevican, neurocan, and versican.
33 roteoglycans as follows: aggrecan, brevican, neurocan, and versican.
34 ary data led us to identify the proteoglycan neurocan as a novel MMP-2 substrate.
35                            Here, we identify neurocan as an astrocyte-secreted inhibitory synaptogeni
36 he extracellular matrix, with hyaluronan and neurocan being removed and not fully replaced after 8 we
37 -comprising proteoglycans (e.g. aggrecan and neurocan), brevican is mainly expressed in the perisynap
38                                 Secretion of neurocan by primary astrocytes and NG2 core protein by N
39                                          The neurocan C-terminal fragment localizes to synapses and c
40 s localized to an NH(2)-terminal fragment of neurocan containing an Ig loop and an HA-binding domain.
41  phosphorylation, glial cell activation, and neurocan deposition after cortical injury.
42 ting regulatory signal for the modulation of neurocan expression in the developing central nervous sy
43  in cultured astrocytes or uninjured cortex, neurocan expression increases significantly in the glial
44                                 Tenascin and neurocan, extracellular matrix molecules that inhibit re
45                                              Neurocan first begins to appear in the spinal cord at E1
46  homology to the mouse and rat proteoglycan, neurocan (GenBank accession Nos X84727 and M97161).
47 quencing of a cosmid containing the complete neurocan gene was performed to determine the genomic str
48  myocyte-specific enhancer factor 2, the rat neurocan gene, and the human cartilage oligomeric matrix
49                                              Neurocan, glypican, or chondroitinase ABC was infused di
50                           Astrocyte-secreted neurocan guides the formation of inhibitory circuits in
51   Similar injections of saline, aggrecan, or neurocan had no significant effect.
52     In early postnatal and adult cerebellum, neurocan immunoreactivity is seen in the prospective whi
53 ve roots, and in the roof plate at E13, when neurocan immunoreactivity is seen only in the mesenchyme
54  vitro, our data suggest that phosphacan and neurocan in areas of reactive gliosis may contribute to
55  a marked increase in the perinatal lectican neurocan in juvenile ADAMTS1 null female frontal cortex.
56 d length of NRs and increased phosphacan and neurocan in MDD and stressed animals suggest that morpho
57 of the neurite outgrowth inhibitors CD44 and neurocan in the degenerative retina, allowing significan
58                                              Neurocan is a chondroitin sulfate proteoglycan thought t
59                                              Neurocan is also expressed by astrocytes in primary cell
60             After secretion from astrocytes, neurocan is cleaved into N- and C-terminal fragments.
61              In vivo, we found that the CSPG neurocan is expressed throughout the alveus, neuropil la
62                Previously we have shown that neurocan is one of the CS-PGs that is upregulated.
63       In the developing chick, neural retina neurocan is present in the inner plexiform layer from da
64                                              Neurocan knockout mice lacking the whole protein or only
65 e discovered that the synaptogenic domain of neurocan localizes to somatostatin-positive inhibitory s
66 short open reading frame in the 5'-leader of neurocan may function as a cis-acting regulatory signal
67                          The distribution of neurocan message is more widespread, extending to the co
68                              The presence of neurocan mRNA in areas where the proteoglycan is not exp
69 and basal telencephalic neuroepithelium, and neurocan mRNA is present in both the ependymal and mantl
70                                              Neurocan mRNA was evident in neurons, including cerebell
71 re the complete coding sequence of the human neurocan mRNA, known as CSPG3, as well as mapping data,
72                          Here, we identified neurocan (NCAN) as a major chondroitin sulfate proteogly
73  phospholipase domain-containing-3 (PNPLA3), neurocan (NCAN), lysophospholipase-like 1 (LYPLAL1), glu
74                                The effect of neurocan on beta1-integrin function is dependent on a si
75  showed behavioral improvement compared with neurocan- or saline-treated rats.
76                  However, maximum binding of neurocan requires both the fibrinogen globe and some of
77 in-specific CSPG genes encoding brevican and neurocan, respectively.
78             The amino acid sequence of human neurocan shows 63% identity with both the mouse and rat
79 ithelial cells of the telencephalon, whereas neurocan staining of brain parenchyma is very weak.
80  proteoglycans (i.e. versican, brevican, and neurocan) substitute for aggrecan, may contribute to the
81 -inhibitory chondroitin sulfate proteoglycan neurocan, the growth-stimulating heparan sulfate proteog
82                    Binding of phosphacan and neurocan to intact tenascin-C, and of phosphacan to the
83  whereas no such effects were seen following neurocan treatment.
84 d dense labeling of the CSPGs NG2, brevican, neurocan, versican, and phosphacan at the host-lesion in
85 chondroitinase treatment, whereas binding of neurocan was not affected.
86               After E18, intense labeling of neurocan was observed in regions of the alveus surroundi
87 n, we injected three purified CSPGs, NG2 and neurocan, which increase in the vicinity of a spinal inj
88 ent with glypican or enzymatic disruption of neurocan with chondroitinase ABC improves gross anatomic
89 tion of the chondroitin sulfate proteoglycan neurocan with its GalNAcPTase receptor coordinately inhi
90 erin and integrin function on interaction of neurocan with its receptor may prevent cell and neurite