Baldwin T J, Lee-Delaunay M B, Knutton S, Williams P H
Department of Genetics, University of Leicester, United Kingdom.
Infect Immun. 1993 Feb;61(2):760-3. doi: 10.1128/iai.61.2.760-763.1993.
Infection of cultured HEp-2 cells with enteropathogenic Escherichia coli causes substantial actin accretion at points of bacterial contact and cell death. Loss of viability was delayed by chelating intracellular free calcium. Actin accretion was partially inhibited by preventing elevation of free cytosolic calcium and prevented by treatment with a calmodulin inhibitor.
用肠致病性大肠杆菌感染培养的人喉表皮样癌细胞(HEp-2细胞)会导致在细菌接触点处大量肌动蛋白积聚以及细胞死亡。通过螯合细胞内游离钙可延迟细胞活力丧失。通过防止游离胞质钙升高可部分抑制肌动蛋白积聚,而用钙调蛋白抑制剂处理则可防止肌动蛋白积聚。