Title : Compound cellular stress maximizes apoptosis independently of p53 in glioblastoma.

Pub. Date : 2022 Jun

PMID : 35311459






3 Functional Relationships(s)
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1 We examined the apoptotic response of two glioblastoma cells, p53 wild type U87 and p53 mutated T98G, to doxorubicin, bortezomib, and vorinostat, which respectively target DNA, 26S proteasome and histone deacetylase, to clarify p53"s function in apoptosis. Doxorubicin tumor protein p53 Homo sapiens
2 We examined the apoptotic response of two glioblastoma cells, p53 wild type U87 and p53 mutated T98G, to doxorubicin, bortezomib, and vorinostat, which respectively target DNA, 26S proteasome and histone deacetylase, to clarify p53"s function in apoptosis. Doxorubicin tumor protein p53 Homo sapiens
3 However, the amounts of p53 in the total count and in the nucleus were much lower with the combination than with doxorubicin alone, suggesting that p53 played no role in either the compound stress, doxorubicin-only or bortezomib-induced apoptosis. Doxorubicin tumor protein p53 Homo sapiens