p53 orchestrates between normal differentiation and cancer.
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Summary
This review aims to provide an over-view of the roles of the key tumor suppressor, p53, in regulating normal differentiation and function of both stem cells and adult cells.
- Type
- article
- Published
- 2015-06-01
- Cited by
- 56
- References
- 158
- OpenAlex
- https://openalex.org/W24406212
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:43513354
Keywords
Political science
References
- Heterogeneity in cancer: cancer stem cells versus clonal evolution.
- Mechanisms maintaining genomic integrity in embryonic stem cells and induced pluripotent stem cells
- Wild type p53 functions as a control protein in the differentiation pathway of the B-cell lineage.
- The tumorigenicity of human embryonic stem cells.
- mdm2 expression is induced by wild type p53 activity.
- Alterations in tumor development in vivo mediated by expression of wild type or mutant p53 proteins.
- DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3.
- Expression of p53 during mouse embryogenesis.
- p53 plays a regulatory role in differentiation and apoptosis of central nervous system-associated cells
- Epithelial-mesenchymal transitions in development and disease.
- NANOG promotes cancer stem cell characteristics and prostate cancer resistance to androgen deprivation
- Snail and Slug Mediate Radioresistance and Chemoresistance by Antagonizing p53‐Mediated Apoptosis and Acquiring a Stem‐Like Phenotype in Ovarian Cancer Cells
- The first 30 years of p53: growing ever more complex
- Distinct regulatory mechanisms and functions of p53-activated and p53-repressed DNA damage response genes in embryonic stem cells
- The tumorigenicity of human embryonic and induced pluripotent stem cells
- Activation of p53 by nutlin leads to rapid differentiation of human embryonic stem cells
- The canals of hering and hepatic stem cells in humans
- When mutants gain new powers: news from the mutant p53 field
- Rescue of early embryonic lethality in mdm2-deficient mice by deletion of p53
- Regulation of p53 in embryonic stem cells.
Cited by
- X-ray and ultraviolet C irradiation-induced γ-H2AX and p53 formation in normal human periosteal cells in vitro: markers for quality control in cell therapy.
- DNA Damage in Stem Cells.
- The p53-Mdm2 loop: a critical juncture of stress response.
- New perspective on targeting the tumor suppressor p53 pathway in the tumor microenvironment to enhance the efficacy of immunotherapy
- Significance of apoptosis related proteins on malignant transformation of ovarian tumors: A comparison between Bcl-2/Bax ratio and p53 immunoreactivity.
- p53 suppression partially rescues the mutant phenotype in mouse models of DiGeorge syndrome
- The paradigm of mutant p53-expressing cancer stem cells and drug resistance.
- Targeting Oncogenic Mutant p53 for Cancer Therapy
- P53 functional abnormality in mesenchymal stem cells promotes osteosarcoma development
- Oncogenic Mutant p53 Gain of Function Nourishes the Vicious Cycle of Tumor Development and Cancer Stem-Cell Formation.
- FoxO proteins or loss of functional p53 maintain stemness of glioblastoma stem cells and survival after ionizing radiation plus PI3K/mTOR inhibition
- Clinical Outcomes of TP53 Mutations in Cancers.
- Lysine methylation represses p53 activity in teratocarcinoma cancer cells
- DNAJA1 controls the fate of misfolded mutant p53 through the mevalonate pathway
- The testis-specific USP26 is a deubiquitinating enzyme of the ubiquitin ligase Mdm2.
- Immunomodulatory Function of the Tumor Suppressor p53 in Host Immune Response and the Tumor Microenvironment
- Differential regulated microRNA by wild type and mutant p53 in induced pluripotent stem cells
- Treatments for EGFR‐mutant non‐small cell lung cancer (NSCLC): The road to a success, paved with failures
- DNA-damage response in hematopoietic stem cells: an evolutionary trade-off between blood regeneration and leukemia suppression.
- p53 and its mutants on the slippery road from stemness to carcinogenesis.
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