High impact information on herbimycin a

• Primary cardiomyocytes were incubated with herbimycin-A or genistein. hsp induction was measured 16-20 h later by Western blotting [1].
• Gelshift analysis demonstrated inhibition of TNF-induced nuclear factor-kappa B (NF-kappa B) mobilization by HMA [2].
• Genistein or HMA did not affect adhesion molecule up-regulation by PMA [2].
• Whereas serum deprivation, butyrate, and herbimycin-A negatively regulated the binding, an extended culture of confluent Caco-2 cells resulted in binding of an additional but as yet unidentified molecule to the Grb2-catalase complex [3].
• Of note, HMA also inhibited LPS-induced IkappaBalpha degradation [4].

Biological context of herbimycin a

• Preincubation with caspase inhibitors protected HMA-induced apoptosis of SC2G cells [5].
• When a human bcl-2 gene was transfected in SC2G cells and overexpressed, SC2G cells seemed to acquire tolerance for HMA [5].
• Decreased beta-catenin phosphorylation through the tyrosine kinase inhibitor herbimycin-A or genistein blocked cell migration, which was accompanied by reorganization of cytoskeletal proteins [6].
• Unlike chemotaxis induced by zymosan-activated human serum, phosphatidate-induced chemotaxis was strongly inhibited by pretreatment of cells with herbimycin-A [7].

Anatomical context of herbimycin a

• We examined the effect of genistein and herbimycin-A, selective inhibitors of tyrosine kinase, on the adherence of human blood neutrophils, lymphocytes, and monocytes to monolayers of human umbilical vein endothelial cells [8].
• These results were further supported by the fact that treatment of monocytes with herbimycin-A, another well-described inhibitor of PTK activity with a different mechanism of action, significantly diminished the effect of M. bovis on CXCL-8 secretion [9].
• Narrow-band UVB-irradiation-induced migration of melanocytes was significantly annihilated by the addition of p125(FAK) inhibitor (herbimycin-A) or MMP-2 inhibitor (GM6001) [10].
• Herbimycin-A-treated human or bovine peripheral blood CD4+ T cells lacked PTK activity and failed to kill virally infected target cells even after cross-killing of CD4 molecules [11].

Associations of herbimycin a with other chemical compounds

• The proteasome inhibitor N-acetyl-leucinyl-leucinyl-norleucinal-H (ALLN) and the tyrosine kinase inhibitor herbimycin A (HMA) blocked A20 mRNA expression and partially inhibited NF-kappaB DNA-binding activity induced by LPS treatment [4].
• Although, doxorubicin and herbimycin-A suppressed [3H]TdR incorporation and induced apoptosis in the Ki-JK cells, they did not induce IL-8 secretion [12].

Gene context of herbimycin a

• In addition, the specificity of this inhibition was demonstrated by the inability of herbimycin-A to block in a significant manner IL-1 beta induction of CXCL-8 [9].
• We conclude that in HUVEC, LPS induces NF-kappaB-dependent genes through degradation of IkappaBalpha, not IkappaBbeta, and propose that this degradation is induced in part by HMA-sensitive kinase(s) upstream of IkappaBalpha [4].
• Terminal deoxyribonucleotidyltransferase-mediated dUTP-biotin nick end labeling and flow cytometric analysis of annexin V staining showed that HMA induced apoptosis of SC2G cells [5].

Analytical, diagnostic and therapeutic context of herbimycin a

• The level of bcl-2 mRNA in SC2G cells was suppressed by HMA in a dose-dependent manner on RT-PCR [5].
• OBJECTIVES: To determine whether pharmacological induction of heat shock proteins (HSPs) by herbimycin-A (a tyrosine-kinase inhibitor) would protect against neutrophil-mediated lung injury in an animal model of lower torso ischaemia-reperfusion [13].

References