The mammalian stress-activated protein p38 mitogen-activated protein kinases (MAPKs) and Jun N-terminal kinases (JNKs) integrate signals that allow cells to interpret a wide range of external signals and respond appropriately by affecting proliferation, differentiation, survival, and migration. p38MAPK and JNK family members play a paradoxical role in cancer and inflammation, eliciting protective responses in some cases and oncogenic or proinflammatory ones in others. Although p38MAPK and JNK family members act in a cell type-specific and cell context-specific manner, the factors that determine which response dominates in a given setting are only partially understood. p38MAPK and JNK have been considered a target for therapeutic intervention in a number of inflammatory disorders, including psoriasis, colitis, and rheumatoid arthritis. We invite authors to submit research and review articles that explore aspects of p38MAPK and JNK signal transduction pathways as they pertain to the physiological responses associated with different pathologies. Potential topics include, but are not limited to:

• Regulation of stress-activated protein kinases
• p38MAPK and JNK and tumorigenesis
• p38MAPK and JNK and immune response
• p38MAPK and JNK and obesity
• Stress-activated protein kinases and transcriptional and translational control
• Interplay of p38MAPK and JNK and other signaling pathways
• Functions of JNK and p38 in development
• JNK and p38 in the cardiac context

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