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- W2024809012 abstract "Cell signalling is carried out by selective and complex metabolic networks that, when impaired, result in disease. The challenge for the cell is to maintain fidelity during normal processes, while allowing the plasticity that is required to control the complicated machinery of a functional cell. This is achieved through protein hubs that organize the flow of information inside the cell; one such hub is the signalling adapter p62 (Moscat et al , 2006). The identification of p62‐interacting proteins, the analysis of knockout (KO) mice, and the fact that p62 mutations are associated with a human disease—Paget bone disease—have confirmed the importance of p62 in homeostatic cell function and disease (Moscat et al , 2007). p62 binds to atypical PKCs, the signalling adapter RIP, the E3 ubiquitin ligase TRAF6, the kinase ERK, and caspase 8 through different motifs (Jin et al , 2009; Moscat et al , 2006), thereby eliciting various effects that …" @default.
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- W2024809012 date "2009-08-01" @default.
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- W2024809012 title "To aggregate or not to aggregate? A new role for p62" @default.
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- W2024809012 doi "https://doi.org/10.1038/embor.2009.172" @default.
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