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. 2017 Sep 29;314(1):H52–H64. doi: 10.1152/ajpheart.00478.2017

Fig. 4.

Fig. 4.

Overexpression of TRAF3 interacting protein 2 (TRAF3IP2), by itself, activates IKKβ/NF-κB and JNK/activator protein 1 (AP-1). A: adenoviral transduction of TRAF3IP2. At 70% confluency, human aortic endothelial cells (HAECs) were infected at the indicated multiplicity of infection (MOI) with an adenoviral vector expressing TRAF3IP2. After 24 h, TRAF3IP2 protein levels were analyzed by immunoblot analysis. B: ectopic expression of TRAF3IP2 activates IKKβ. HAECs infected with Ad.TRAF3IP2 (MOI 10 for 24 h) or incubated with TPCA-1 (5 µM in DMSO) were analyzed for IKKβ activation by immunoblot analysis. C: ectopic expression of TRAF3IP2 activates NF-κB via IKKβ and IκB degradation. HAECs treated as in B but with TPCA-1 (5 µM in DMSO) or MG-132 (5 µM in DMSO) were analyzed for NF-κB activation by immunoblot analysis using activation-specific anti-p65 antibodies. D: ectopic expression of TRAF3IP2 activates JNK. HAECs infected with Ad.TRAF3IP2 (MOI 10 for 24 h) and incubated with SP600125 (20 µM in DMSO for 30 min) were analyzed for JNK activation by immunoblot analysis. E: ectopic expression of TRAF3IP2 activates AP-1 via JNK. HAECs treated as in D were analyzed for AP-1 activation by immunoblot analysis using activation-specific anti-c-Jun antibodies. Bar graphs in A–E represent densitometric analyses from 3 independent experiments. *P ≤ 0.05 vs. control (i.e., open bar); †P ≤ 0.05 vs. HG (n = 3).