Title : Gallic acid induces apoptosis of lung fibroblasts via a reactive oxygen species-dependent ataxia telangiectasia mutated-p53 activation pathway.

Pub. Date : 2010 Mar 10

PMID : 20151649






6 Functional Relationships(s)
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1 Gallic acid induces apoptosis of lung fibroblasts via a reactive oxygen species-dependent ataxia telangiectasia mutated-p53 activation pathway. Gallic Acid ataxia telangiectasia mutated Mus musculus
2 Mechanistic studies showed that gallic acid induces early phosphorylation of p53(Ser18) and histone 2AX(Ser139) (H2AX) via ataxia telangiectasia mutated (ATM) activation in response to ROS-provoked DNA damage. Gallic Acid ataxia telangiectasia mutated Mus musculus
3 Mechanistic studies showed that gallic acid induces early phosphorylation of p53(Ser18) and histone 2AX(Ser139) (H2AX) via ataxia telangiectasia mutated (ATM) activation in response to ROS-provoked DNA damage. Gallic Acid ataxia telangiectasia mutated Mus musculus
4 When mouse lung fibroblasts were treated with caffeine, an ATM kinase inhibitor, the levels of p53, phosphorylated p53(Ser18), and cell death induced by gallic acid were significantly attenuated. Gallic Acid ataxia telangiectasia mutated Mus musculus
5 Additionally, pretreatment with antioxidants drastically inhibited the gallic acid-induced 8-hydroxy-2"-deoxyguanosine (8-OH-dG) formation and phosphorylation of p53(Ser18) and ATM(Ser1981), as well as apoptosis. Gallic Acid ataxia telangiectasia mutated Mus musculus
6 Our results provide the first evidence of the activation of ROS-dependent ATM/p53 signaling as a critical mechanism of gallic acid-induced cell death in primary cultured mouse lung fibroblasts. Gallic Acid ataxia telangiectasia mutated Mus musculus