| Name | syndecans |
|---|---|
| Synonyms | CD138; CD138 antigen; Heparan sulfate proteoglycan fibroblast growth factor receptor; SDC; SDC 1; SDC1; SYND 1; SYND1… |
| Name | sodium chlorate |
|---|---|
| CAS | sodium chlorate |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 11006575 | Sebestyen A, Totth A, Mihalik R, Szakacs O, Paku S, Kopper L: Syndecan-1-dependent homotypic cell adhesion in HT58 lymphoma cells. Tumour Biol. 2000 Nov-Dec;21(6):349-57. In the case of heparitinase/trypsin digestion with long-term inhibition of HS synthesis (sodium chlorate treatment), the inhibited aggregation was accompanied by cell cycle arrest and the induction of apoptosis. |
7(0,0,0,7) | Details |
| 11262187 | Borgenstrom M, Tienhaara A, Spillmann D, Salmivirta M, Jalkanen M: -induced growth of S115 mouse mammary tumor cells is dependent on Exp Cell Res. 2001 Apr 1;264(2):307-14. We have previously shown that overexpression of syndecan-1 heparan sulfate proteoglycan renders S115 cells insensitive to and now demonstrate that this effect can be overcome by sodium chlorate treatment in combination with exogenous |
6(0,0,1,1) | Details |
| 19812150 | Kalia M, Chandra V, Rahman SA, Sehgal D, Jameel S: Heparan sulfate proteoglycans are required for cellular binding of the hepatitis E virus ORF2 capsid protein and for viral infection. J Virol. 2009 Dec;83(24):12714-24. Epub 2009 Oct 7. Using an approximately 56-kDa recombinant pORF2 that can self-assemble as virus-like particles, we demonstrated that cell surface heparan sulfate proteoglycans (HSPGs), specifically syndecans, play a crucial role in the binding of pORF2 to Huh-7 liver cells. Removal of cell surface by enzymatic (heparinase) or chemical (sodium chlorate) treatment of cells or competition with and their oversulfated derivatives caused a marked reduction in pORF2 binding to the cells. |
3(0,0,0,3) | Details |
| 12761845 | Ford-Perriss M, Turner K, Guimond S, Apedaile A, Haubeck HD, Turnbull J, Murphy M: Localisation of specific heparan sulfate proteoglycans during the proliferative phase of brain development. Dev Dyn. 2003 Jun;227(2):170-84. We find that FGF2 stimulation of proliferation is inhibited in the presence of sodium chlorate, an inhibitor of synthesis, and is rescued by addition of exogenous Syndecan-1 and glypican-4 were the most highly expressed in the developing brain during the time of peak proliferation and localise to ventricular regions of the brain, where the precursor cells are proliferating. |
1(0,0,0,1) | Details |
| 18372231 | Levallet G, Levallet J, Bonnamy PJ: FSH-induced phosphoprotein phosphatase 2A-mediated deactivation of particulate phosphodiesterase-4 activities is abolished after alteration in proteoglycan synthesis in immature rat Sertoli cells. J Endocrinol. 2008 Apr;197(1):45-54. Both the FSH-induced increase in recruitment/activation of particulate PP2A and the subsequent deactivation of particulate PDE4 were abolished when Sertoli cell proteoglycans (PGs) synthesis was altered by sodium chlorate. Particularly, developmentally regulated transmembrane syndecans, the most abundant PGs in Sertoli cells, by targeting PP2A at the membrane level could allow developmental control of activated particulate PDE4s and, potentially, other signaling phosphoproteins, including the FSH receptor, during the early postnatal period. |
1(0,0,0,1) | Details |
| 11856308 | Brucato S, Bocquet J, Villers C: Cell surface heparan sulfate proteoglycans: target and partners of the basic fibroblast growth factor in rat Sertoli cells. Eur J Biochem. 2002 Jan;269(2):502-11. Indeed, sodium chlorate, described to drastically decrease proteoglycan sulfation, abolishes the bFGF downregulation of FSH-stimulated synthesis previously observed. Glypican-1, syndecan-1 and -4, potential bFGF coreceptors, are mainly regulated at the transcriptional level. |
1(0,0,0,1) | Details |
| 8444842 | Tyrrell DJ, Ishihara M, Rao N, Horne A, Kiefer MC, Stauber GB, Lam LH, Stack RJ: Structure and biological activities of a -derived hexasaccharide with high affinity for basic fibroblast growth factor. J Biol Chem. 1993 Mar 5;268(7):4684-9. The hexasaccharide effectively inhibits the binding of syndecan-transfected RO-12 UC cells to bFGF-coated wells (Ishihara, M., Tyrrell, D.J., Kiefer, M.C., Barr, P.J., and Swiedler, S.J. (1992) Anal. Unlike the from which it was derived, however, the hexasaccharide cannot promote the binding of 125I-bFGF to a recombinant high affinity bFGF receptor (flg) or restore the bFGF-dependent proliferative response to ACE cells grown in the presence of 5 mM sodium chlorate. |
1(0,0,0,1) | Details |
| 17081280 | Djanani A, Mosheimer B, Kaneider NC, Ross CR, Ricevuti G, Patsch JR, Wiedermann CJ: Heparan sulfate proteoglycan-dependent neutrophil chemotaxis toward PR-39 cathelicidin. J Inflamm. 2006 Nov 2;3:14. Modification of heparan sulfate proteoglycans with sodium chlorate inhibited migration whereas chemotaxis toward the chemoattractant formyl-Met-- was not affected. Involvement of syndecans is likely as both heparinase and chondroitinase were abrogating. |
1(0,0,0,1) | Details |
| 15292202 | Gingis-Velitski S, Zetser A, Kaplan V, Ben-Zaken O, Cohen E, Levy-Adam F, Bashenko Y, Flugelman MY, Vlodavsky I, Ilan N: Heparanase uptake is mediated by cell membrane heparan sulfate proteoglycans. J Biol Chem. 2004 Oct 15;279(42):44084-92. Epub 2004 Jul 29. Co-localization studies and cell fractionation following heparanase addition have identified syndecan family members as candidate molecules responsible for heparanase uptake, providing an efficient mechanism that limits extracellular accumulation and function of heparanase. Addition of or xylosides to cell cultures resulted in a pronounced accumulation of, heparanase in the culture medium, whereas sodium chlorate had no such effect. |
1(0,0,0,1) | Details |