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• W2023182523 abstract "The epithelium of mucosal and skin surfaces serves as a permeability barrier and affords mechanisms for local immune defense. Crucial to the development and maintenance of a properly functioning epithelium is the balance of cell proliferation, differentiation, and death. Here we show that this balance depends on cross-regulatory interactions among multiple protein kinase-mediated signals and their coordinated transmission. From an investigation of conditional gene knock-out mice, we find that epithelial-specific loss of the protein kinase p38α leads to aberrant activation of TAK1, JNK, EGF receptor, and ERK in distinct microanatomical areas of the intestines and skin. Consequently, the epithelial tissues display excessive proliferation, inadequate differentiation, and sensitivity to apoptosis. These anomalies leave the tissue prone to damage and collapse at the trigger of an environmental insult. The vulnerability of p38α-deficient epithelium predicts adverse effects of long term pharmacological p38α inhibition; yet such limitations could be overcome by concomitant blockade of one or more of the dysregulated protein kinase signaling pathways.Background: The protein kinase p38α mediates cellular responses to stress and immune signals.Results: Loss of p38α in epithelial cells results in aberrant activation of multiple protein kinases and disrupts tissue homeostasis.Conclusion: Epithelial tissue homeostasis requires cross-regulatory interactions between p38α and other protein kinases.Significance: These findings provide clues about how to prevent the adverse effects of p38 inhibitors. The epithelium of mucosal and skin surfaces serves as a permeability barrier and affords mechanisms for local immune defense. Crucial to the development and maintenance of a properly functioning epithelium is the balance of cell proliferation, differentiation, and death. Here we show that this balance depends on cross-regulatory interactions among multiple protein kinase-mediated signals and their coordinated transmission. From an investigation of conditional gene knock-out mice, we find that epithelial-specific loss of the protein kinase p38α leads to aberrant activation of TAK1, JNK, EGF receptor, and ERK in distinct microanatomical areas of the intestines and skin. Consequently, the epithelial tissues display excessive proliferation, inadequate differentiation, and sensitivity to apoptosis. These anomalies leave the tissue prone to damage and collapse at the trigger of an environmental insult. The vulnerability of p38α-deficient epithelium predicts adverse effects of long term pharmacological p38α inhibition; yet such limitations could be overcome by concomitant blockade of one or more of the dysregulated protein kinase signaling pathways. Background: The protein kinase p38α mediates cellular responses to stress and immune signals. Results: Loss of p38α in epithelial cells results in aberrant activation of multiple protein kinases and disrupts tissue homeostasis. Conclusion: Epithelial tissue homeostasis requires cross-regulatory interactions between p38α and other protein kinases. Significance: These findings provide clues about how to prevent the adverse effects of p38 inhibitors." @default.
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• W2023182523 date "2013-08-01" @default.
• W2023182523 modified "2023-10-07" @default.
• W2023182523 title "Tuning of Protein Kinase Circuitry by p38α Is Vital for Epithelial Tissue Homeostasis" @default.
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• W2023182523 doi "https://doi.org/10.1074/jbc.m113.452029" @default.
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