Title : Cross-talk of alpha tocopherol-associated protein and JNK controls the oxidative stress-induced apoptosis in prostate cancer cells.

Pub. Date : 2013 May 15

PMID : 23129185






4 Functional Relationships(s)
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1 Further mechanistic study showed exposure of prostate cancer cells to H(2)O(2) resulted in increased phosphorylation of both JNK and c-Jun, and TAP siRNA effectively decreased H(2)O(2) -induced JNK and c-Jun phosphorylation. Hydrogen Peroxide Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
2 Further mechanistic study showed exposure of prostate cancer cells to H(2)O(2) resulted in increased phosphorylation of both JNK and c-Jun, and TAP siRNA effectively decreased H(2)O(2) -induced JNK and c-Jun phosphorylation. Hydrogen Peroxide Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
3 Further mechanistic study showed exposure of prostate cancer cells to H(2)O(2) resulted in increased phosphorylation of both JNK and c-Jun, and TAP siRNA effectively decreased H(2)O(2) -induced JNK and c-Jun phosphorylation. Hydrogen Peroxide Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
4 Further mechanistic study showed exposure of prostate cancer cells to H(2)O(2) resulted in increased phosphorylation of both JNK and c-Jun, and TAP siRNA effectively decreased H(2)O(2) -induced JNK and c-Jun phosphorylation. Hydrogen Peroxide Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens