Title : Singlet oxygen-induced activation of Akt/protein kinase B is independent of growth factor receptors.

Pub. Date : 2003 Oct

PMID : 14626664






6 Functional Relationships(s)
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1 Exposure of fibroblasts to 1O2 elicited a strong and sustained phosphorylation of Akt, which occurred concurrently with phosphorylation of p38 kinase, a proapoptotic signal. CHEBI:63768 thymoma viral proto-oncogene 1 Mus musculus
2 Significantly, cell death induced by 1O2 was enhanced by inhibition of PI3-K, suggesting that activation of Akt by 1O2 may contribute to fibroblast survival under this form of oxidative stress. CHEBI:63768 thymoma viral proto-oncogene 1 Mus musculus
3 Significantly, cell death induced by 1O2 was enhanced by inhibition of PI3-K, suggesting that activation of Akt by 1O2 may contribute to fibroblast survival under this form of oxidative stress. CHEBI:63768 thymoma viral proto-oncogene 1 Mus musculus
4 Activation of neither focal adhesion kinase (FAK) nor Ras protein, both of which mediate responses to reactive oxygen species, appeared to be pathways for the 1O2-induced activation of the PI3-K-Akt survival pathway. CHEBI:63768 thymoma viral proto-oncogene 1 Mus musculus
5 Thus, activation of Akt by 1O2 is mediated by PI3-K and contributes to a survival response that counteracts cell death after 1O2-induced injury. CHEBI:63768 thymoma viral proto-oncogene 1 Mus musculus
6 However, unlike the response to other oxidants, activation of the PI3-K-Akt by 1O2 does not involve activation of growth factor receptors, FAK or Ras protein. CHEBI:63768 thymoma viral proto-oncogene 1 Mus musculus