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1 protein tyrosine phosphatase beta (RPTPbeta)/phosphacan.
2 revican, and neurocan, and downregulation of phosphacan.
3  distribution of LeX is more restricted than phosphacan.
4 molecules, glycolipids, and the proteoglycan phosphacan.
5  O-mannosyl glycan modifications on RPTPzeta/phosphacan.
6 gand binding assay we have demonstrated that phosphacan, a chondroitin sulfate proteoglycan of nervou
7 n, which was identified by immunoblotting as phosphacan, a CSPG abundant in adult brain.
8 e chondroitin sulfate chains on neurocan and phosphacan account for at least 80% of their binding to
9                         We identify DSD-1-PG/phosphacan, an extracellular matrix component associated
10  with the deposition of unprocessed DSD-1-PG/phosphacan and excessive Timm-positive, mossy fiber term
11 te outgrowth in vitro, our data suggest that phosphacan and neurocan in areas of reactive gliosis may
12          Reduced length of NRs and increased phosphacan and neurocan in MDD and stressed animals sugg
13                                   Binding of phosphacan and neurocan to intact tenascin-C, and of pho
14 of isoAsp may be important in the roles that phosphacan and other CSPGs play in development of the ne
15 posed to the fibrinogen globe in mixtures of phosphacan and tenascin-C.
16 iochemically distinct glycoforms of RPTPzeta/phosphacan and that these glycoforms differentially deco
17 rations of 10 microg protein/ml, both native phosphacan and the core protein obtained by chondroitina
18  gene that include the extracellular form of phosphacan and the transmembrane receptor protein tyrosi
19 ed on a minor isoform/glycoform of RPTPzeta (phosphacan) and is found in the extracellular milieu of
20 its catalytically inactive, secreted isoform phosphacan, and this interaction was regulated during de
21                                 Neurocan and phosphacan are also high affinity ligands of amphoterin
22                                Both forms of phosphacan are made by astrocytes, suggesting that kerat
23 ary shadowing electron micrographs that show phosphacan as a rod terminated at one end by a globular
24 CSPGs NG2, brevican, neurocan, versican, and phosphacan at the host-lesion interface after spinal cor
25 d binding assays and inhibition studies that phosphacan binding is retained in all deletion variants
26 mphoterin also produces a 5-fold increase in phosphacan binding to the neural cell adhesion molecule
27                                              Phosphacan binding was decreased by approximately 70% fo
28 e lacking the fibrinogen-like globe and that phosphacan binds to this single domain with nearly the s
29                     Conversely, Neurocan and Phosphacan broadly decrease with time in all models.
30                                 Neurocan and phosphacan can be localized to reactive astrocytes 30 d
31 nked glycans released from purified RPTPzeta/phosphacan demonstrated that this protein is a significa
32 n was inhibited by similar concentrations of phosphacan, demonstrating that the fibrinogen globe is n
33  also exhibit the laminar band and DSD- 1-PG/phosphacan deposition, but mossy fiber outgrowth through
34 plain some of the complex binding properties phosphacan exhibits with its natural ligands.
35 ed a biphasic expression, while Neurocan and Phosphacan expression declined dramatically with time an
36 onstrate that the expression of neurocan and phosphacan follow different developmental time courses n
37 le, consistent with recent observations that phosphacan forms a tight complex with tenascin-R.
38 ed by the presence of splice variants of the phosphacan gene that include the extracellular form of p
39 es on the proteoglycan, N-deglycosylation of phosphacan had no effect on its binding to TAG-1/axonin-
40 Purkinje cell, and molecular layers, whereas phosphacan immunoreactivity is associated with Bergmann
41                                              Phosphacan immunostaining and levels were increased in b
42 wed an overlapping localization of FGF-2 and phosphacan in the developing central nervous system.
43 ve compared the distribution of neurocan and phosphacan in the developing central nervous system.
44 he O-linked glycan heterogeneity of RPTPzeta/phosphacan in the early postnatal mouse brain by multidi
45 a decrease in the expression of aggrecan and phosphacan in the pericontusional cortex with a concomit
46 r nervous tissue proteoglycans, neurocan and phosphacan, in embryonic and postnatal rat brain and spi
47                            Moreover, whereas phosphacan interactions with certain proteins are mediat
48                                              Phosphacan is also widely distributed in embryonic spina
49                                     The CSPG phosphacan is expressed primarily in the neuropil layers
50 protein-tyrosine phosphatase zeta (RPTPzeta)/phosphacan is hypoglycosylated in a mouse model of one o
51 inal zone and subplate of the neocortex, and phosphacan is present in the ventricular zone and also h
52 E16-19, strong staining of both neurocan and phosphacan is seen in the marginal zone and subplate of
53 ot been extensively studied in the CNS where phosphacan is the only protein that appears to contain K
54 own KSPGs (aggrecan, claustrin, SV2, ABAKAN, phosphacan-KS), indicating that 5D4 is labeling KSPGs no
55  suggests that hypoglycosylation of RPTPzeta/phosphacan may have different functional consequences in
56                                 In contrast, phosphacan message was detected only in astroglia, such
57                                  The average phosphacan molecule in adult brain contains at least sev
58                      At embryonic day 13-16, phosphacan mRNA is largely confined to areas of active c
59 is apparently mediated by a direct action of phosphacan on the cells rather than by its interaction w
60                                 In contrast, phosphacan protein levels are decreased in the glial sca
61 ondroitin sulfate proteoglycans neurocan and phosphacan/protein-tyrosine phosphatase-zeta/beta were f
62                   At embryonic day 13 (E13), phosphacan surrounds the radially oriented neuroepitheli
63                            We could validate phosphacan, tenascin-C, and L1-CAM as major LeX carrier
64 ndroitin sulfate proteoglycans, neurocan and phosphacan (the extracellular domain of protein-tyrosine
65 ulfate chains to the binding of neurocan and phosphacan to TAG-1/axonin-1 is therefore the opposite o
66 ly 75% in the absence of calcium, binding of phosphacan to tenascin-R was not affected by the absence
67 an and neurocan to intact tenascin-C, and of phosphacan to the fibrinogen globe, is significantly inc
68  FORSE-1 and an antibody to the proteoglycan phosphacan, which carries LeX, shows that the distributi
69 ondroitin sulfate proteoglycans neurocan and phosphacan with the extracellular matrix protein tenasci
70 ferences in the interactions of neurocan and phosphacan with the two major members of the tenascin fa