Abstract：
:Mutations of the retinoblastoma tumor suppressor, pRb, or its cyclin-cyclin-dependent kinase (CDK) regulatory kinases or CDK inhibitors, allows unrestrained E2F activity, leading to unregulated cell cycle progression. However, overexpression of E2F-1 also sensitizes cells to apoptosis, suggesting that targeting this pathway may be of therapeutic benefit. Enforced expression of E2F-1 in interleukin-3-dependent myeloid cells led to preferential sensitivity to the topoisomerase II inhibitor, etoposide, which was independent of p53 accumulation. Pretreatment of the E2F-1-expressing cells with ICRF-193, a second topoisomerase II inhibitor that does not cause DNA damage, protected these cells against etoposide-induced apoptosis. However, ICRF-193 cooperated with other DNA-damaging agents to induce apoptosis. Enforced expression of E2F-1 led to accumulation of p53 protein. An E2F-1 mutant that is defective in inducing cell cycle progression also induced p53, suggesting that p53 was responding directly to E2F, and not to secondary events caused by inappropriate cell cycle progression (i.e., DNA damage). Thus, topoisomerase II inhibition and DNA damage cooperate to selectively induce apoptosis in cells that have mutations in the pRb pathway.
journal_name
Cell Biochem Biophysjournal_title
Cell biochemistry and biophysicsauthors
Nip J,Hiebert SWdoi
10.1385/CBB:33:2:199subject
Has Abstractpub_date
2000-01-01 00:00:00pages
199-207issue
2eissn
1085-9195issn
1559-0283pii
CBB:33:2:199journal_volume
33pub_type
杂志文章abstract：:There is an emergent need for improving the microsurgical technique of variant arterial anastomosis to reduce the often seen surgery-related complications. We describe in this article our experience in improving this technique, in 73 living donor liver grafts (64 right lobes, 9 left lobes) in patients with end-stage l...
journal_title：Cell biochemistry and biophysics
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