Tyrphostin AG30
(Synonyms: 酪氨酸磷酸化抑制剂AG30,AG30) 目录号 : GC38125Tyrphostin AG30 (AG30), a potent and selective EGFR tyrosine kinase inhibitor, selectively inhibits self renewal induction by c-ErbB, and is able to inhibit activation of STAT5 by c-ErbB in primary erythroblasts.
Cas No.:122520-79-0
Sample solution is provided at 25 µL, 10mM.
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Tyrphostin AG30 (AG30), a potent and selective EGFR tyrosine kinase inhibitor, selectively inhibits self renewal induction by c-ErbB, and is able to inhibit activation of STAT5 by c-ErbB in primary erythroblasts.
[1] Wessely O, et al. Cell Growth Differ. 1997 May;8(5):481-93.
Cas No. | 122520-79-0 | SDF | |
别名 | 酪氨酸磷酸化抑制剂AG30,AG30 | ||
Canonical SMILES | O=C(/C(C#N)=C/C1=CC=C(C(O)=C1)O)O | ||
分子式 | C10H7NO4 | 分子量 | 205.17 |
溶解度 | DMSO: 125 mg/mL (609.25 mM) | 储存条件 | Store at -20°C |
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Distinct roles of the receptor tyrosine kinases c-ErbB and c-Kit in regulating the balance between erythroid cell proliferation and differentiation
Cell Growth Differ 1997 May;8(5):481-93.PMID:9149900doi
In the bone marrow, multipotent and committed hematopoietic progenitors have to closely regulate their balance between sustained proliferation without differentiation (self renewal) and entering a terminal differentiation pathway. A useful model to analyze this regulation at the molecular level is committed avian erythroid progenitors. These are induced to undergo long-term self renewal by the ligand-activated receptor tyrosine kinase (RTK) c-ErbB, in cooperation with steroid hormone receptors. This self-renewal induction by c-ErbB even occurs in the presence of differentiation factors (erythropoietin and insulin). Under the same conditions, the RTK c-Kit is unable to sustain erythroid progenitor self renewal, stimulating cell proliferation without arresting terminal differentiation. Two mechanisms are involved in these differential activities of c-Kit and c-ErbB. The first one, differential regulation of receptor expression, proved to be of minor importance, because c-Kit was unable to induce self renewal, even if exogenously expressed from a retrovirus at high levels. Rather our results support the second mechanism, i.e., that receptor-specific signal transduction is responsible for the differential biological activity of c-Kit and c-ErbB: (a) specific tyrosine kinase inhibitors (tryphostins) were found which selectively inhibited the biological function of either c-Kit or c-ErbB in erythroblasts but did not affect ligand-induced autophosphorylation of either RTK; and (b) c-ErbB selectively induced SHC phosphorylation and STAT5 activation. The Ras pathway was similarly activated by c-Kit and c-ErbB. The c-ErbB-specific Tyrphostin AG30 specifically blocked STAT5 activation, implicating this signal transducer in c-ErbB-induced self renewal.