| Target Validation Information | |||||
|---|---|---|---|---|---|
| Target ID | T36121 | ||||
| Target Name | Myc proto-oncogene protein | ||||
| Target Type | Research |
||||
| Drug Potency against Target | TWS-119 | Drug Info | IC50 = 15000 nM | [527964] | |
| Action against Disease Model | Resten-MP | In a porcine coronary model, an advanced c-myc-eluting PC stent loaded with AVI-4126 using soak trap blocked c-myc expression and significantly inhibited myointimal hyperplasia and allowed complete reendothelialization and healing response. | [552259] | Drug Info | |
| The Effect of Target Knockout, Knockdown or Genetic Variations | Proto-oncogenes such as c-myc have been implicated in the regulation of cellular proliferation and differentiation, and in the heart the switch from myocyte proliferation to terminal differentiation is synchronous with a decrease in c-myc mRNA abundance. To determine whether c-myc can influence myocyte proliferation or differentiation, we examined the in vivo effect of increasing c-myc expression during embryogenesis and of preventing the decrease in c-myc mRNA expression that normally occurs during cardiac development. The model system used was a strain of transgenic mice exhibiting constitutive expression of c-myc mRNA in cardiac myocytes throughout development. In these transgenic mice, increased c-myc mRNA expression was found to be associated with both atrial and ventricular enlargement. This increase in cardiac mass was secondary to myocyte hyperplasia, with the transgenic hearts containing more than twice as many myocytes as did nontransgenic hearts. The results suggest that in the transgenic animals there is additional hyperplastic growth during fetal development. However, this additional proliferative growth is not reflected in abnormal myocyte maturation, as assessed by the expression of the cardiac and skeletal isoforms of alpha-actin. The results of this study indicate that constitutive expression of c-myc mRNA in the heart during development results in enhanced hyperplastic growth and suggest a regulatory role for this proto-oncogene in cardiac myogenesis | [552259] | |||
| References | |||||
| Ref 552259 | P-selectin antagonism with recombinant p-selectin glycoprotein ligand-1 (rPSGL-Ig) inhibits circulating activated platelet binding to neutrophils induced by damaged arterial surfaces. J Pharmacol Exp Ther. 2001 Aug;298(2):658-64. | ||||
| Ref 527964 | Nat Chem Biol. 2005 Jul;1(2):74-84.Diversity-oriented synthesis: exploring the intersections between chemistry and biology. | ||||
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