Disease relevance of AG 213

• Pre-incubation of monocytes with tyrphostin-A47 reduced the binding of B. pertussis to such monocytes as well [1].
• BACKGROUND AND OBJECTIVES: We propose that a growth factor receptor tyrosine kinase (RTK) inhibitor, such as tyrphostin A47, could serve as an adjunct to estrogen replacement therapy (ERT) for postmenopausal breast cancer survivors [2].

High impact information on AG 213

• The protein tyrosine kinase inhibitor tyrphostin RG50864, which blocks EGF-dependent cell proliferation, blocked EGF-induced tyrosine phosphorylation of PLC-II, its association with EGF receptor, and EGF-induced Ca2+ release [3].
• Induction of mitogenesis was not the major contribution of bFGF and VEGF165 because the cell number did not change significantly in the presence of TNFalpha, and tyrphostin A47, which inhibited mitosis completely, reduced the formation of tubular structures only by 28-36% [4].
• When cultures were subjected to E fields in the presence of a tyrosine kinase inhibitor, tyrphostin RG-50864, cathodal AChR clustering was abolished with a half maximal inhibitory dosage of 50 microM [5].
• Continuous infusion of RG-50864, an inhibitor of EGF receptor kinase activity, at the site of injury prevented the advancement of puberty induced by the lesion [6].
• Herbimycin A also reduced PAI-1 synthesis, but several other tyrosine protein kinase inhibitors, namely tyrphostin A47, methyl-2,5-dihydroxy-cinnamate, and compound 5, were unable to do so [7].

Biological context of AG 213

• Tyrphostin (RG 50864), a compound reported to inhibit specifically the EGF receptor kinase, completely blocked EGF stimulation of proto-oncogene induction [8].
• 4. The inhibitory action of alpha-cyano-3,4-dihydroxythiocinnamamide was found to be at or upstream of phospholipase C activation, blocking both phosphatidylinositol hydrolysis and protein kinase C activation. alpha-Cyano-3,4-dihydroxythiocinnamamide did not affect agonist receptor binding sites or receptor affinity in neutrophils [9].
• IFN-gamma induced significantly higher cell survival compared to that of unexposed cultures, and this survival could be suppressed by incubation with the tyrosine protein kinase (TPK) specific inhibitor tyrphostin A47 at the non-toxic concentration of 10(-6) M [10].
• Using a representative tyrphostin, A47, the validity of MTT assay as a measure of cell proliferation was tested by a colony formation assay and by immunostaining with Ki-67 antibodies [11].
• To test whether EGF effects the timing and positional information required for limb-specific cartilage morphogenesis, we employed tyrphostin (RG 50864) which inhibits EGF receptor kinase activity in a concentration-dependent manner and severely retards limb development [12].

Anatomical context of AG 213

• The same concentration of AG 213 interfered with HUVEC focal adhesion and stress fiber formation [13].
• 3. In the presence of cytochalasin B, FMLP stimulated elastase release from neutrophils was also inhibited to unstimulated levels by 5 min pretreatment with alpha-cyano-3,4-dihydroxythiocinnamamide [9].
• We studied the effects of a tyrphostin derivative, RG 50864, without preincubation in intact epithelial cells [14].
• RG 50864, in a dose-dependent manner, inhibited EGF-dependent development of 2-cell embryos to blastocysts and the number of cells per blastocyst [15].
• Tyrphostin-A47 inhibitable tyrosine phosphorylation of flagellar proteins is associated with distinct alteration of motility pattern in hamster spermatozoa [16].

Associations of AG 213 with other chemical compounds

• In ionophore-stimulated cells, the inhibition of the 110-kDa protein tyrosine phosphorylation and serotonin release by RG 50864 occurs in parallel [17].
• However, pretreatment with PTK inhibitors genistein, tyrphostin A25, and tyrphostin A47 blocked the volume-activated taurine efflux [18].
• Two unrelated tyrosine kinase inhibitors, tyrphostin RG-50864 and herbimycin A, were both very efficient blockers of IL-3-dependent lipid mediator formation whereas C5a-induced histamine release was preserved [19].
• 2. alpha-Cyano-3,4-dihydroxythiocinnamamide dose-dependently inhibited intracellular calcium release and superoxide generation from human neutrophils activated by 1 microM LTB4, PAF, and FMLP [9].

Gene context of AG 213

• Unexpectedly, treatment of NIH3T3 cells with both tyrphostin (RG 50864) and EGF results in an increase in the level of tyrosine phosphorylation of the MAP kinase [20].
• Epidermal growth factor receptor signaling cascade as target for tyrphostin (RG 50864) in epithelial cells. Paradoxical effects on mitogen-activated protein kinase kinase and mitogen-activated protein kinase activities [14].
• Activation of the mitogen-activated protein kinase cascade by tyrphostin (RG 50864) [20].
• By contrast, BSA enhanced the selective inhibition of TGF alpha-stimulated DNA synthesis by tyrphostin A47 [21].
• This induction was also inhibited by a tyrosine kinase inhibitor, tyrphostin RG-50864, suggesting the role of receptor tyrosine kinase activation in this process [22].

References