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Nuclear factor kappa-B and the heart

Guro Valen, MD, PhD^*, Zhong-qun Yan, PhD and G.öran K. Hansson, MD, PhD

^* Crafoord Laboratory of Experimental Surgery, Karolinska Hospital, Stockholm, Sweden
Center of Molecular Medicine, Karolinska Hospital, Stockholm, Sweden

View larger version (31K): [in a new window]   Figure 1 A schematic presentation of activation of the transcription nuclear factor kappa-B (NFB). In the cytoplasm of the resting cell, the NFB dimer, often consisting of the subunits p50/p65, is bound to inhibitory proteins known as inhibitory kappa-B (IB). Stimuli activating IB kinases will cause nuclear translocation of the NFB dimer, while IB is proteolytically degraded. In the nucleus, NFB binds to consensus sites in promoter/enhancer regions of genes it regulates, and transcription of these substances commences. COX-2 = cyclo-oxygenase-2 inhibitor; ICAM-2 = intercellular adhesion molecule 2; IL = interleukin; iNOS = inducible nitric oxide synthase; LPS = lipopolysaccharide; MHC = major histocompatibility complex; TNF = tumor necrosis factor; VCAM-1 = vascular cell adhesion molecule-1.