A variation in the structure of the protein-coding region of the human p53 gene

Buchman, Vladimir L.; Chumakov, Peter M.; Ninkina, Natalia; Samarina, O. P.; Georgiev, G.P.

doi:10.1016/0378-1119(88)90196-5

Cited by 244 publications

(100 citation statements)

References 28 publications

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“…However, the p53 sequences analysed from HMEC 184 displayed a homozygous arginine residue at codon 72. This previously characterized germline polymorphism at codon 72, which contains either an arginine (CGC) or a proline residue (CCC), has been observed at this position in the p53 sequence of several human p53 clones derived from normal and transformed cells (Matlashewski et al, 1987;Buchman et al, 1988). Therefore, these data con®rm that HMEC184 contain a wild-type p53 protein.…”

Section: Hmec184 Contain Wild-type P53mentioning

confidence: 56%

Human mammary epithelial cells exhibit a differential p53-mediated response following exposure to ionizing radiation or UV light

et al. 1999

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The tumor suppressor protein, p53, plays a critical role as a transcriptional activator of downstream target genes involved in the cellular response to DNA damaging agents. We examined the cell cycle checkpoint response of human mammary epithelial cells (HMEC) and their isogenic ®broblast counterparts to ionizing (IR) and ultraviolet (UV) radiation, two genotoxic agents whose DNA damage response pathways involve p53. Using¯ow cytometric analysis, we found that both mortal and immortalized HMEC, which contain wild-type p53 sequence, do not exhibit a G1 arrest in response to IR, but show an intact G2 checkpoint. Supportive evidence from Western analyses revealed that there was neither an increase in p53 nor one of its downstream targets, p21 WAF1 , in HMEC exposed to IR. In contrast, isogenic mammary ®broblasts arrest at the G1 checkpoint and induce the p53 and p21 WAF1 proteins following IR. By comparison, HMEC exposed to UV displayed an S phase arrest and induced the expression of p53 and p21 WAF1 . Our results show that the cellular response to DNA damage depends on both the type of damage introduced into the DNA and the speci®c cell type.

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Section: Hmec184 Contain Wild-type P53mentioning

confidence: 56%

Human mammary epithelial cells exhibit a differential p53-mediated response following exposure to ionizing radiation or UV light

et al. 1999

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“…[4][5][6] Unfortunately, at the time of its discovery, researchers were inadvertently studying a tumor-derived mutant form of p53, with the belief that TRP53 was an oncogene. Therefore, the only functional analysis performed for these polymorphic variants was for their transforming potential, which did not differ, so the polymorphism was deemed functionally insignificant.…”

Section: Polymorphisms In Tp53: the Codon 72 Polymorphismmentioning

confidence: 99%

Polymorphic variants in the p53 pathway

Murphy

2006

Cell Death Differ

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“…8 (outer). and 8 (inner) were prepared according to the sequence published by Buchman et al (1988 (1998) 78(3), 354-359 (38%). These 16 tumours had mutations in each of the analysed exons as follows: exon 5 in six tumours, exon 6 in five tumours, exon 7 in four tumours and exon 8 in four tumours.…”

Section: Analysis Of P53 Mutations By Nested Pcr-sscpmentioning

confidence: 99%

p53 mutations and human papillomavirus DNA in oral squamous cell carcinoma: correlation with apoptosis

Koh

Cho²,

Kong³

et al. 1998

Br J Cancer

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Summary Forty-two oral squamous cell carcinomas (SCCs) were analysed for p53 mutations and human papillomavirus (HPV) (Regezi et al. 1993). W'hereas the epidemiology has been w-ell described so far. the molecular steps involsed in the pathogenesis of these common neoplasms are poorly understood. The role of human papillomas-irus (HPV) in the development of anogenital cancers has been widely studied. and current evidence shows that HPV infection is necessars for the desvelopment of most cervical cancers (zur Hausen. 1994). Approximately 80-90% of cervical carcinomas contain HPV DNA. and the predominant or high-risk types appear to be HPV-16. -18 and -33 (Yoshikawa et al. 1991). HPV E6 and E7 proteins. consistentlv expressed in HPV-transformed and HPVpositive tumours. can exert their oncogenic potential bv inactivating the products of the p53 tumour-suppressor cene (Lemine. 1990: zur Hausen. 1994) and the retimoblastoma (Rb) grene (Dy-son et al. 1989). In oral malignant lesions. the state of HPV infection has been reported to be as high as 76%c (Snijders et al. 1994). although there are still conflicting results in infection rate and role of HPV in oral carcinorenesis.

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A variation in the structure of the protein-coding region of the human p53 gene

Cited by 244 publications

References 28 publications

Human mammary epithelial cells exhibit a differential p53-mediated response following exposure to ionizing radiation or UV light

Human mammary epithelial cells exhibit a differential p53-mediated response following exposure to ionizing radiation or UV light

Polymorphic variants in the p53 pathway

p53 mutations and human papillomavirus DNA in oral squamous cell carcinoma: correlation with apoptosis

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