Tumor necrosis factor receptor (TNFR)-associated factors (TRAFs) are a family of structurally related proteins that transduces signals from members of TNFR superfamily and various other immune receptors. Major downstream signaling events mediated by the TRAF molecules include activation of the transcription factor nuclear factor κB (NF-κB) and the mitogen-activated protein kinases (MAPKs). In addition, some TRAF family members, particularly TRAF2 and TRAF3, serve as negative regulators of specific signaling pathways, such as the noncanonical NF-κB and proinflammatory toll-like receptor pathways. Thus, TRAFs possess important and complex signaling functions in the immune system and play an important role in regulating immune and inflammatory responses. This review will focus on the role of TRAF proteins in the regulation of NF-κB and MAPK signaling pathways.

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Background: KLF4 is essential for VSMC differentiation induced by ATRA. Results: RAR␣ interacts with KLF4-Sp1-YB1 bound to the Klf4 promoter and transactivates Klf4 in VSMCs in a RAREindependent manner. Conclusion: RAR␣ functions as a co-activator of KLF4-Sp1-YB1 complex. Significance: These results described a novel mechanism of regulation of Klf4 by ATRA and RAR␣.

HighlightsKrüppel-like factor 4 (KLF4) was downregulated in breast cancer tissues.KLF4 was upregulated in TNF-α–stimulated SK-BR-3 breast cancer cells.KLF4 inhibited proliferation and promoted apoptosis in breast cancer cells.Overexpression of KLF4 suppressed SK-BR-3 cell tumorigenicity in vivo.