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JNK activation can result in subsequent phosphorylation of multiple nuclear substrates that can include transcription factor c-Jun, activating transcription factor 2 (ATF2), p53, and others, and further stimulate downstream targets and contribute to stress response through alterations in the cell cycle, DNA damage repair, and/or programmed cell death [59]

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Access this article Similar content being viewed by others References Moldawer LL, Sattler FR (1998) Human immunodeficiency virus-associated wasting and mechanisms of cachexia associated with inflammation

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