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Your search keyword '"Tumor Suppressor Protein p53 physiology"' showing total 2 results
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2 results on '"Tumor Suppressor Protein p53 physiology"'

1. Genetic evidence of a role for ATM in functional interaction between human T-cell leukemia virus type 1 Tax and p53

Author

Kyong-Wook Yim, Phillip L. Van, Dong-Yan Jin, Kuan-Teh Jeang, George Dapolito, and Akihiro Kurimasa

Subjects
Immunology, Cell Cycle Proteins, Ataxia Telangiectasia Mutated Proteins, DNA-Activated Protein Kinase, Protein Serine-Threonine Kinases, Gene Products, tax - physiology, CREB, medicine.disease_cause, Microbiology, Jurkat cells, Transformation and Oncogenesis, Protein-Serine-Threonine Kinases - physiology, Virology, medicine, Humans, Nuclear protein, Phosphorylation, Cyclic AMP Response Element-Binding Protein, Tumor Suppressor Protein p53 - physiology, Mutation, Human T-lymphotropic virus 1, biology, Tumor Suppressor Proteins, Human T-lymphotropic virus 2, Human T-lymphotropic virus 1 - physiology, NF-kappa B, Nuclear Proteins, Gene Products, tax, biology.organism_classification, NFKB1, Molecular biology, Cell biology, DNA-Binding Proteins, Repressor Proteins, Cell culture, Insect Science, biology.protein, Tumor Suppressor Protein p53, HeLa Cells
Abstract

Recent evidence from several investigators suggest that the human T-cell leukemia virus type 1 Tax oncoprotein represses the transcriptional activity of the tumor suppressor protein, p53. An examination of published findings reveals serious controversy as to the mechanism(s) utilized by Tax to inhibit p53 activity and whether the same mechanism is used by Tax in adherent and suspension cells. Here, we have investigated Tax-p53 interaction simultaneously in adherent epithelial (HeLa and Saos) and suspension T-lymphocyte (Jurkat) cells. Our results indicate that Tax activity through the CREB/CREB-binding protein (CBP), but not NF-κB, pathway is needed to repress the transcriptional activity of p53 in all tested cell lines. However, we did find that while CBP binding by Tax is necessary, it is not sufficient for inhibiting p53 function. Based on knockout cell studies, we correlated a strong genetic requirement for the ATM, but not protein kinase-dependent DNA, protein in conferring a Tax-p53-repressive phenotype., published_or_final_version

Published
2000

2. Prognostic significance of p53 in the cancer of the larynx

Author

Assimakopoulos, D., Evangelos Kolettas, Zagorianakou, N., Evangelou, A., Skevas, A., and Agnantis, N. J.

Subjects
p53, wild-type, over-expression, DNA-damage, Laryngeal Neoplasms/*genetics/*pathology, squamous-cell carcinoma, Genes, p53, Tumor Suppressor Protein p53/*physiology, epithelial lesions, tumor-suppressor gene, Humans, laryngeal cancer, molecular analysis, prognosis, protein expression, neck-cancer, binding-site
Abstract

lp53 is a nuclear phosphoprotein acting as . transcription factor to regulate cell cycle progression and apoptosis, mediated by a number of target genes, p53 mutant proteins have lost a) the ability to act as sequence-specific transcription factors and b) their tumour suppressive properties. As p53 is the most commonly mutated gene in human cancer including laryngeal squamous cell carcinoma, an aggressive and most frequent tumour of head and neck, it has attracted a great deal of interest as a prognostic factor diagnostic tool and therapeutic tar-get. This article reviews the current understanding of the prognostic significance of p53 in laryngeal squamous cell carcinoma. Immunohistochemical staining techniques and molecular generics demonstrated thar p53 activation is an early event in laryngeal squamous cell carcinogenesis but can not be used as a reliable prognostic marker. Anticancer Research

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