BIOL 4215 Lecture Notes - Lecture 1: Type Three Secretion System, Proliferating Cell Nuclear Antigen, Shigella Flexneri
Document Summary
Shigella ipgb1 promotes bacterial entry through the elmo-dock180 machinery. Ipgb1 recruits host gef to the membrane: the gef is elmo dock180 complex, bacterial protein recruits a gef resulting in polymerization of the actin cytoskeleton. Escape into cytoplasm: pore forming toxins ipab and ipac insert into vacuole membrane (cholesterol dependent) to cause degradation. Ipab and ipac also help to form pore and insert into membrane to put in injectosome: function of ipab and. Icsb protein protects shigella from autophagy autophagy targets virg. Organelle that isn"t functioning, around what they want to get rid of; building phagosome around it ex. bacteria, unfolded proteins; autophagasome can bind with lysosome: initiation, elongation, maturation/flux, atg5 binds virg and targets the organism for autophagy. Iscb shares the same binding site with atg5 on virg and allows escape from destruction from autophagy: atg5 binding to virg is competitively inhibited by icsb. Vira on shigella is a protease that is capable of severing the microtubule.
