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Fig. 2 | Journal of Biomedical Science

Fig. 2

From: SUMO proteins in the cardiovascular system: friend or foe?

Fig. 2

Participation of SUMOylation in molecular signalling pathways involved in atherosclerosis. In the NFκB pathway, SUMOylation of IκBα via SUMO1 proves atheroprotective while IκBα SUMO2/3 conjugation proves atherogenic and so does NEMO SUMOylation. MK2 SUMOylation inhibits VCAM1/MCP1 mediated inflammation acting as a friend while p53 SUMOylation is apoptotic, hence SUMOylation acts as a foe here. SUMO when bound to MAGI activates p30RSK which further stabilizes ERK–SUMO interaction by retaining SENP2 in the cytoplasm, hence SUMOylation here in both the scenarios prove to be hazardous to the cells. Bcl2 B cell lymphoma 2, CO carbon monoxide, d flow distributed flow, ERK5 extracellular-signal-regulated kinase 5, HO hemeoxygenase, IκBα inhibitor of κB-α, IκK inhibitor of κB kinase, Klf Kruppel-like Factor, MAGI membrane-associated guanylate kinase with inverted domain structure-1, MCP1 monocyte chemoattractant protein 1, MK2 mitogen-activated protein kinase-activated protein kinase 2, NEMO NFκB essential modulator, P90RSK P90 Ribosomal s6 Kinase, PIASγ protein inhibitor of activated STAT γ, PKCζ protein kinase C ζ, PPAR peroxisome proliferator-activated receptor, s flow steady flow, SENP sentrin/SUMO-specific proteases, SMRT1 silencing mediator of retinoic acid and thyroid hormone receptor, VCAM vascular cell adhesion protein

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