Participation of p53 protein in the cellular response to DNA damage.
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Summary
A role for the wild-type p53 protein in the inhibition of DNA synthesis that follows DNA damage is suggested and a new mechanism for how the loss of wild- type p53 might contribute to tumorigenesis is suggested.
- Type
- article
- Published
- 1991-12-01
- Cited by
- 3,996
- References
- 51
- OpenAlex
- https://openalex.org/W1847864430
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:11995070
Keywords
DNA damage, Biology, Progenitor cell, Carcinogenesis, DNA repair
References
- Human p53 is phosphorylated by p60-cdc2 and cyclin B-cdc2.
- Isolation of RNA.
- Spontaneous abnormalities in normal fibroblasts from patients with Li-Fraumeni cancer syndrome: aneuploidy and immortalization.
- Activating mutations for transformation by p53 produce a gene product that forms an hsc70-p53 complex with an altered half-life
- Effects of morpholinyl doxorubicins, doxorubicin, and actinomycin D on mammalian DNA topoisomerases I and II.
- Two distinct mechanisms regulate the levels of a cellular tumor antigen, p53
- Oligomerization of oncoprotein p53
- The RAD9 gene controls the cell cycle response to DNA damage in Saccharomyces cerevisiae.
- Prospective study of a family cancer syndrome.
- Wild-type p53 can inhibit oncogene-mediated focus formation.
- Major deletions in the gene encoding the p53 tumor antigen cause lack of p53 expression in HL-60 cells.
- A genetic model for colorectal tumorigenesis.
- Mechanism by which caffeine potentiates lethality of nitrogen mustard.
- Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms.
- The action of caffeine on X-irradiated HeLa cells. I. Delayed inhibition of DNA synthesis.
- A technique for radiolabeling DNA restriction endonuclease fragments to high specific activity.
- T antigen is bound to a host protein in SY40-transformed cells
- Tumor suppressor genes.
- Cell proliferation in carcinogenesis.
- The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53.
Cited by
- Differential p53 protein expression in breast cancer fine needle aspirates: the potential for in vivo monitoring
- Genetic alterations in adult diffuse glioma: occurrence, significance, and prognostic implications.
- Mechanisms of resistance to alkylating agents.
- Demonstration of DNA damage/repair in individual cells using in situ end labelling: Association of p53 with sites of DNA damage
- Immunohistochemical detection of p53 protein in mammary carcinoma: an important new independent indicator of prognosis?
- Androgen ablation-induced programmed death of prostatic glandular cells does not involve recruitment into a defective cell cycle or p53 induction.
- p53, Rb and bcl-2 expression during the cell cycle: a study in phytohaemagglutinin stimulated lymphocytes and microwave irradiated lymphoid tissue sections.
- Defining origins of replication in mammalian cells.
- Overexpression of p53 and long-term survival in colon carcinoma.
- p53 protein in low-grade astrocytomas: a study with long-term follow-up.
- Lymphocyte death, p53, and the problem of the "undead" cell.
- The tumor suppressor p53 modifies mutational processes in a human lymphoblastoid cell line.
- Signal transduction and apoptosis pathways as therapeutic targets.
- Epithelial apoptosis
- Potential applications of cell cycle manipulation to clinical response.
- Apoptosis was promoted at a nonpermissive temperature in DNA replication-defective temperature-sensitive mutants of mouse FM3A cells.
- Multisite phosphorylation and the integration of stress signals at p53.
- Induction of apoptosis by taxol and cisplatin and effect on cell cycle-related proteins in cisplatin-sensitive and -resistant human ovarian cells.
- Up-regulation of inducible nitric oxide synthase expression in cancer-prone p53 knockout mice.
- Disruption of actin microfilaments by cytochalasin D leads to activation of p53
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