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Editorial
. 2010 Apr 1;86(1):1-3.
doi: 10.1093/cvr/cvq026. Epub 2010 Jan 25.

Ubiquitin, a novel paracrine messenger of cardiac cell survival

Dan Li, Christophe Depre
Editorial

Ubiquitin, a novel paracrine messenger of cardiac cell survival

Dan Li et al. Cardiovasc Res. .
No abstract available

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Figures

Figure 1
Figure 1
Hypothetical mechanism by which extracellular ubiquitin modulates the survival function of Akt. The hypothesis is that the mechanism of extracellular release and cellular reuptake of ubiquitin in cardiac myocytes exposed to cell stress will direct these ubiquitin units to specific UbK63-E3 ligases, thereby activating intracellular cascades sustaining cardiac cell survival by blocking pro-apoptotic effectors and activating anti-apoptotic effectors. This mechanism would be totally independent of the one by which Akt participates in cardiac cell growth through activation of translation that is linked to proteasome-associated proteolysis by the UbK48 ubiquitination process. casp-9, caspase-9; GFR, growth factor receptor; GPCR, G protein-coupled receptor; HSP, heat shock proteins; NOS, nitric oxide synthase; PDK1, phosphatidylinositol-dependent kinase 1; PI3K, phosphatidylinositol 3-kinase; u, ubiquitin.
See this image and copyright information in PMC

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