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The fragment abundance increased in a biphasic manner, peaking at 6\u20109\u00a0hours and 48\u00a0hours post infection. Treatment of LU cells with calpain inhibitors eliminated most detectable p53 fragments. In cell\u2010free experiments, exogenous m\u2010calpain cleavage generated p53(\u0394Cp44). Attempts to preserve p53 proteins by treating cells with the calpain inhibitor E64d for 6\u00a0hours before harvesting increased the sensitivity of p53 to calpain cleavage. p53 in mock\u2010infected cell lysates was much more sensitive to cleavage and degradation by exogenous calpain than that in HCMV\u2010infected cells. The proteasome inhibitor MG132 stabilized p53(\u0394Cp44), particularly in mock\u2010infected cells. p53(\u0394Cp44) appeared to be tightly associated with a chromatin\u2010rich fraction. The abundance of p53\u03b2 was unchanged over a 96\u2010h time course and very similar in mock\u2010 and HCMV\u2010infected cells, making it unlikely that p53(\u0394Cp44) was p53\u03b2. The biological activities of this and other fragments lacking C\u2010terminal sequences are unknown, but deserve further investigation, given the association of p53(\u0394Cp44) with the chromatin\u2010rich (or buffer C insoluble) fraction in HCMV\u2010infected cells.<\/jats:p>","DOI":"10.1096\/fba.1028","type":"journal-article","created":{"date-parts":[[2019,3,25]],"date-time":"2019-03-25T11:01:49Z","timestamp":1553511709000},"page":"151-166","source":"Crossref","is-referenced-by-count":5,"title":["Calpain\u2010mediated cleavage of p53 in human cytomegalovirus\u2010infected lung fibroblasts"],"prefix":"10.1096","volume":"1","author":[{"given":"Zhenping","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology University of Texas Medical Branch Galveston Texas"},{"name":"Department of Pathology University of Texas Medical Branch Galveston Texas"},{"name":"Department of Surgery University of Texas Medical Branch Galveston 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