Titlebook: Nuclear Factor кB; Regulation and Role Rudi Beyaert Book 2003 Kluwer Academic Publishers 2003 Mammalia.apoptosis.biology.biomedicine.cell.

incontinence

Valves

NF-,B in Genetic Disorders,h as inflammatory cytokines, bacterial lipopolysaccharide (LPS), viral infection or stress, I.B is phosphorylated on two critical serine residues. This modification allows its recognition and destruction via the proteasome degradation machinery. As a consequence, free NF-.B enters the nucleus and ac

Semblance

NF-,B in the Vascular System,, more generally, stress-response reactions. In this regard, the vascular wall that represents one of the main barriers in the organism, namely the interface between blood and underlying tissue, is of outstanding importance. The vascular wall consists mainly of endothelial cells (EC) and smooth musc

Diuretic

Commonplace

NF-,B in the Nervous System,us system was first described in 1993, consisting of inducible DNA-binding complexes composed of p50 and p65 subunits (Kaltschmidt et al., 1993b). This evidence and the already well-characterized role of NF-.B in the immune system and in inflammation prompted us to propose potential roles of NF-.B i

Negligible

NF-,B in Oncogenesis and As a Target for Cancer Therapy,ses in cancer. The roles for NF-.B in cancer appear to be complex and likely involve the ability of this transcription factor to control apoptosis, cell-cycle progression, cell differentiation, angiogenesis and cell migration. Consistent with its role in oncogenesis, NF-.B is activated by most oncop

進(jìn)取心

Control of Immunity by Rel Proteins in Drosophila,ree main strategies (Tzou et al., 2002). The first is activation of proteolytic cascades that lead to coagulation and melanization once the cuticle has been injured. This reaction, during which blood clotting occurs and Phenoloxydase converts dopamine to melanin, is thought to limit the pathogen dis

botany

Leisureliness

合并

NF-,B Activation by Tumor Necrosis Factor and Interleukin-1,o-immune diseases (Aggarwal et al., 2000). IL-1 has been found to be one of the most powerful endogenous pyrogens involved in the same physiological phenomena as TNF, except for tumor modulation (Dinarello et al., 2000a–b).