| Name | fibroblast growth factor 2 |
|---|---|
| Synonyms | BFGF; BHBGF 2; BHBGF2; Basic fibroblast growth factor; FGF; FGF2; FGFB; Fibroblast growth factor 2… |
| Name | sodium chlorate |
|---|---|
| CAS | sodium chlorate |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. 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. |
37(0,1,1,7) | Details |
| 7672514 | Chen JK, Chao HH, Yang VC: Inhibition of the growth of a human nasopharyngeal carcinoma cell line by bFGF is mediated via FGFR-1. FASEB J. 1995 Sep;9(12):1211-9. The biological effect of bFGF is conveyed through its binding to the high-affinity receptor sites and the binding is dependent on the presence of cell surface -like molecules, as treatment of cells with heparitinase or sodium chlorate abolishes high-affinity binding and growth inhibition. |
37(0,1,1,7) | Details |
| 9748322 | Sperinde GV, Nugent MA: Heparan sulfate proteoglycans control intracellular processing of bFGF in vascular smooth muscle cells. Biochemistry. 1998 Sep 22;37(38):13153-64. HSPG-deficient VSMC were generated by treating cells with sodium chlorate to inhibit the sulfation of HSPG. |
10(0,0,0,10) | Details |
| 9278150 | Schriever C, Breithardt G, Schmidt A: Undersulfation of proteoheparan stimulates the expression of basic fibroblast growth factor and protein synthesis but suppresses replication of coronary smooth muscle cells. Biol Chem. 1997 Jul;378(7):701-6. When cultured cSMC were treated with 10 mM sodium chlorate in -depleted medium, the cell number and [3H] incorporation decreased by 76% and 66% respectively, while the protein content per cell was doubled. |
5(0,0,0,5) | Details |
| 1646484 | Rapraeger AC, Krufka A, Olwin BB: Requirement of for bFGF-mediated fibroblast growth and myoblast differentiation. Science. 1991 Jun 21;252(5013):1705-8. |
4(0,0,0,4) | Details |
| 8663512 | Fannon M, Nugent MA: Basic fibroblast growth factor binds its receptors, is internalized, and stimulates DNA synthesis in Balb/c3T3 cells in the absence of J Biol Chem. 1996 Jul 26;271(30):17949-56. In our studies, Balb/c3T3 fibroblasts were treated with 50 mM sodium chlorate to completely inhibit (99%) sulfation of proteoglycans. |
3(0,0,0,3) | Details |
| 8725286 | Choy M, Oltjen SL, Otani YS, Armstrong MT, Armstrong PB: Fibroblast growth factor-2 stimulates embryonic cardiac mesenchymal cell proliferation. Dev Dyn. 1996 Jun;206(2):193-200. Inhibition of sulfation of cell surface glycosaminoglycans by treatment with sodium chlorate significantly reduced both the formation of the fibronectin matrix and cell proliferation in response to FGF-2, suggesting an involvement of the low-affinity sulfated glycosaminoglycan FGF receptor system. |
2(0,0,0,2) | Details |
| 7577706 | Laslett AL, McFarlane JR, Hearn MT, Risbridger GP: Requirement for proteoglycans to mediate basic fibroblast growth factor (FGF-2)-induced stimulation of Leydig cell steroidogenesis. J Steroid Biochem Mol Biol. 1995 Sep;54(5-6):245-50. This stimulatory action on basal steroidogenesis is mediated through HSPG, as it was blocked by the addition of (100 micrograms/ml), sodium chlorate (25mM) and protamine sulphate (5 micrograms/ml). |
2(0,0,0,2) | Details |
| 10736179 | Sperinde GV, Nugent MA: Mechanisms of fibroblast growth factor 2 intracellular processing: a kinetic analysis of the role of heparan sulfate proteoglycans. Biochemistry. 2000 Apr 4;39(13):3788-96. HSPG-deficient cells were generated by treatment with sodium chlorate. |
2(0,0,0,2) | Details |
| 8986623 | Delehedde M, Deudon E, Boilly B, Hondermarck H: Heparan sulfate proteoglycans play a dual role in regulating fibroblast growth factor-2 mitogenic activity in human breast cancer cells. Exp Cell Res. 1996 Dec 15;229(2):398-406. To investigate the potential regulation of FGF-2 mitogenic activity by heparan sulfate proteoglycans (HSPG), we have treated human breast cancer cells by glycosaminoglycan degrading enzymes or a metabolic inhibitor of proteoglycan sulfation: sodium chlorate. |
2(0,0,0,2) | Details |
| 17706452 | Nikitovic D, Assouti M, Sifaki M, Katonis P, Krasagakis K, Karamanos NK, Tzanakakis GN: and -containing proteoglycans are both partners and targets of basic fibroblast growth factor-mediated proliferation in human metastatic melanoma cell lines. Int J Biochem Cell Biol. 2008;40(1):72-83. Epub 2007 Jul 30. Treatment with the specific inhibitor of the glycosaminoglycan sulfation, sodium chlorate, demonstrated that endogenous glycosaminoglycan/proteoglycan production is required for both basal and stimulated by FGF-2 proliferation of these cells. |
2(0,0,0,2) | Details |
| 10022972 | Molteni A, Modrowski D, Hott M, Marie PJ: Alterations of matrix- and cell-associated proteoglycans inhibit osteogenesis and growth response to fibroblast growth factor-2 in cultured rat mandibular condyle and calvaria. Cell Tissue Res. 1999 Mar;295(3):523-36. In this study, we used 4-methylumbelliferyl-beta-d-xyloside, an inhibitor of PG synthesis, and sodium chlorate, a competitive inhibitor of glycoconjugate sulfation, to determine the functional consequences of alterations of PG metabolism on osteogenesis and on FGF actions in neonatal rat condyle and calvaria in vitro. |
1(0,0,0,1) | Details |
| 11257129 | Fedorov YV, Rosenthal RS, Olwin BB: Oncogenic Ras-induced proliferation requires autocrine fibroblast growth factor 2 signaling in skeletal muscle cells. J Cell Biol. 2001 Mar 19;152(6):1301-5. Oncogenic Ras-induced proliferation is abolished by addition of an anti-FGF-2 blocking antibody, suramin, or treatment with either sodium chlorate or heparitinase, demonstrating an autocrine requirement for FGF-2. |
1(0,0,0,1) | Details |
| 8950517 | Zhu X, Sasse J, McAllister D, Lough J: Evidence that fibroblast growth factors 1 and 4 participate in regulation of cardiogenesis. Dev Dyn. 1996 Dec;207(4):429-38. Evidence that this represented FGF receptor-mediated signaling rather than a nonspecific effect of exogenous FGF was indicated by the ability of sodium chlorate to inhibit FGF-mediated cardiogenesis. Previous studies in this laboratory have indicated that the early embryonic chick heart depends on fibroblast growth factor-2 (FGF-2; bFGF), sequentially utilized in paracrine and autocrine fashion, for its growth and development (Sugi and Lough, [1995] Dev. |
1(0,0,0,1) | Details |
| 14517424 | Natke B, Venkataraman G, Nugent MA, Sasisekharan R: Heparinase treatment of bovine smooth muscle cells inhibits fibroblast growth factor-2 binding to fibroblast growth factor receptor but not FGF-2 mediated cellular proliferation. Angiogenesis. 1999;3(3):249-57. On the surface of smooth muscle cells there are two types of receptors for the mitogenic and angiogenic growth factor fibroblast growth factor-2 (FGF-2); a high affinity tyrosine kinase FGF receptor (FGFR1) and low affinity /heparan-like glycosaminoglycan (HLGAG) component of surface expressed proteoglycans. Through the use of both sodium chlorate and FGF-2 mutants with deficient HLGAG-binding capabilities, we show the FGF-2-HLGAG interaction is important for FGF-2's ability to induce SMC proliferation. |
1(0,0,0,1) | Details |
| 10961890 | Salek-Ardakani S, Arrand JR, Shaw D, Mackett M: and bind interleukin-10 and modulate its activity. Blood. 2000 Sep 1;96(5):1879-88. Glycosaminoglycans (GAG) are a group of negatively charged molecules that have been shown to bind and directly regulate the bioactivity of growth factors and cytokines such as basic fibroblast growth factor, transforming growth factor-beta, IL-7, and interferon-gamma. |
1(0,0,0,1) | Details |
| 9191974 | Laslett AL, McFarlane JR, Risbridger GP: Developmental response by Leydig cells to acidic and basic fibroblast growth factor. J Steroid Biochem Mol Biol. 1997 Feb;60(3-4):171-9. These effects were mediated by -proteoglycans (HSPG), as they were blocked by the addition of protamine sulphate and sodium chlorate. |
1(0,0,0,1) | Details |
| 9693150 | Godin RE, Takaesu NT, Robertson EJ, Dudley AT: Regulation of BMP7 expression during kidney development. Development. 1998 Sep;125(17):3473-82. Treatment of whole kidneys with sodium chlorate to disrupt proteoglycan synthesis results in the loss of BMP7 expression in the mesenchyme whereas expression in the epithelial components of the kidney are unaffected. In addition, we have used this reporter allele to analyze the expression of BMP7 in response to several known survival factors (EGF, bFGF) and inducers of metanephric mesenchyme, including the ureteric bud, spinal cord and LiCl. |
1(0,0,0,1) | Details |
| 8550829 | Faber-Elman A, Solomon A, Abraham JA, Marikovsky M, Schwartz M: Involvement of wound-associated factors in rat brain astrocyte migratory response to axonal injury: in vitro simulation. J Clin Invest. 1996 Jan 1;97(1):162-71. The soluble substances, applied to the scratch-wounded astrocytes, blocked their migration whereas some known wound-associated factors such as transforming growth factor-beta 1 (TGF-beta 1), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha), and -binding epidermal growth factor in combination with insulin-like growth factor-1 (HB-EGF + IGF-1) stimulated intensive migration with consequent closure of the wound. |
1(0,0,0,1) | Details |
| 14966081 | Newman DR, Li CM, Simmons R, Khosla J, Sannes PL: affects signaling pathways stimulated by fibroblast growth factor-1 and -2 in type II cells. Am J Physiol Lung Cell Mol Physiol. 2004 Jul;287(1):L191-200. Epub 2004 Feb 13. a model for sulfated components of basement membrane matrices, is known to inhibit fibroblast growth factor (FGF)-2-stimulated DNA synthesis as well as gene expression of FGF-2 and its receptor in AT2 cells. In addition, experiments were done on cells grown in the presence of 20 mM sodium chlorate (sulfation inhibitor). |
1(0,0,0,1) | Details |
| 8652906 | Delehedde M, Deudon E, Boilly B, Hondermarck H: [Involvement of sulfated proteoglycans in the control of proliferation of MCF-7 breast cancer cells]. Bull Cancer. 1996 Feb;83(2):129-34. The MCF-7 breast cancer cells exhibit remarkable growth enhancement in response to basic fibroblast growth factor (FGF-2) stimulation in a dose dependent manner. Sodium chlorate treatment reduced by 70% sulfation of proteoglycans. |
1(0,0,0,1) | Details |
| 12423248 | Deguchi Y, Okutsu H, Okura T, Yamada S, Kimura R, Yuge T, Furukawa A, Morimoto K, Tachikawa M, Ohtsuki S, Hosoya K, Terasaki T: Internalization of basic fibroblast growth factor at the mouse blood-brain barrier involves perlecan, a heparan sulfate proteoglycan. J Neurochem. 2002 Oct;83(2):381-9. Moreover, the -resistant binding of [125I] bFGF in TM-BBB4 cells was significantly reduced by 50% following treatment with sodium chlorate, suggesting the loss of perlecan (a core protein of heparan sulfate proteoglycan, HSPG) from the extracellular matrix of the cells. |
89(1,1,1,9) | 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. |
91(1,1,1,11) | Details |
| 8050494 | Gannoun-Zaki L, Pieri I, Badet J, Barritault D: Interaction of basic fibroblast growth factor (FGF-2) with nonresponsive HeLa cells. Exp Cell Res. 1994 Aug;213(2):375-82. |
6(0,0,0,6) | Details |
| 7840621 | Chintala SK, Miller RR, McDevitt CA: Role of in the terminal differentiation of growth plate chondrocytes. Arch Biochem Biophys. 1995 Jan 10;316(1):227-34. Treatment of growth plate chondrocytes with sodium chlorate, a reversible inhibitor of glycosaminoglycan sulfation, resulted in terminal differentiation of growth plate chondrocytes even in the presence of bFGF at concentrations that normally repress their differentiation. |
87(1,1,1,7) | Details |
| 10684625 | Fannon M, Forsten KE, Nugent MA: Potentiation and inhibition of bFGF binding by a model for regulation of cellular response. Biochemistry. 2000 Feb 15;39(6):1434-45. Balb/c3T3 cells were treated with various concentrations of sodium chlorate, so as to express a range of endogenous sites, and [(125) I] bFGF binding was assessed in the presence of a range of concentrations. |
39(0,1,1,9) | Details |