Structural Biochemistry/Viruses and SLiMs Interaction/ Viral Pathways/ Manipulating Signal Transduction

Manipulating Signal Transduction
SLiMs have low-binding compatibility which enable them to react fast and produce decision-making functions due to changing stimuli in the cell. Because of their abilities to response to changing stimuli, a lot of signaling networks depend on the motif interactions with their modular domains “such as SH2, SH3 and PDZ”. Viruses take advantage on this ability by imitating signaling motifs to alter and deregulate the pathways the motifs take. A model of such a virus is known as EBV latent membrane protein 1 (LMP1). This viral protein “is a constitutively active ligand-independent mimic of host factor CD40, and contains motifs that mediate the recruitment of Janus kinase 3 (JAK3) (PxxPxP275&302), TNFRSF1A-associated via death domain (TRADD) (YYD-COOH384) and several TNF receptor-associated factors (TRAF) (PxQxT204), collectively required for activation of nuclear factor-kappa B (NF-kB) signaling, blocking apoptosis and driving B cell proliferation”. Apoptosis is the mechanism that leads to  cell  death and  cell proliferation is the mechanism that drives an increase in the number of cells as a result of cell growth and cell division.