Maintenance of genomic integrity by p53: complementary roles for activated and non-activated p53

Albrechtsen, Nils; Dornreiter, Irena; Grosse, Frank; Kim, Ella; Wiesmüller, Lisa; Deppert, Wolfgang

doi:10.1038/sj.onc.1202952

Cited by 164 publications

(134 citation statements)

References 144 publications

(115 reference statements)

Supporting

Mentioning

119

Contrasting

Unclassified

Order By: Relevance

“…In order to elicit a productive infection, viral DNA ampli®cation needs to be controlled and it is plausible that the activity of E6* could ensure the presence of a limited amount of p53 at the replication sites, where it could both prevent overreplication of the viral genome and, possibly, assist DNA synthesis by means of its proofreading capacity. Indeed, HPV recruits DNA polymerase a for DNA replication, and the 3' ± 5' exonuclease activity of p53 could enhance the replicative ®delity of this enzyme (for review, Albrechtsen et al, 1999). It is interesting to note that p53 has been found in the replication centres of Herpes Simplex Virus (Wilcock and Lane, 1991), Cytomegalovirus (Fortunato and Spector, 1998) and Adenovirus (KoÈ nig et al, 1999), and recent studies reported an interaction between the HPV ori-complex binding protein E2 and p53, further suggesting a potential positive role for p53 in viral replication (Massimi et al, 1999).…”

Section: Interactions Between Hpv E6 and P53mentioning

confidence: 99%

The Human Papillomavirus E6 protein and its contribution to malignant progression

2001

View full text Add to dashboard Cite

The Human Papillomavirus (HPV) E6 protein is one of three oncoproteins encoded by the virus. It has long been recognized as a potent oncogene and is intimately associated with the events that result in the malignant conversion of virally infected cells. In order to understand the mechanisms by which E6 contributes to the development of human malignancy many laboratories have focused their attention on identifying the cellular proteins with which E6 interacts. In this review we discuss these interactions in the light of their respective contributions to the malignant progression of HPV transformed cells. Oncogene (2001) 20, 7874 ± 7887.

show abstract

Section: Interactions Between Hpv E6 and P53mentioning

confidence: 99%

The Human Papillomavirus E6 protein and its contribution to malignant progression

2001

View full text Add to dashboard Cite

show abstract

“…Besides transcriptional regulation, there have only been a limited number of descriptions on other p53 functions, for example, complex formation (Bates and Vousden, 1999). One other such function is the direct role of p53 in DNA repair, which in part stems from its exonuclease activity (Mummenbrauer et al, 1996;Albrechtsen et al, 1999). Taken together, the main contribution of p53 in growth arrest and apoptosis control appears to originate from its transcriptional activity, by both activation and repression of target genes.…”

Section: Introductionmentioning

confidence: 99%

Identification of Tcf-4 as a transcriptional target of p53 signalling

et al. 2004

View full text Add to dashboard Cite

“…A primary mechanism by which p53 negatively controls the cell cycle is through the transcriptional activation of p21, which is a protein with the function of retaining the cell cycle at the R point, thereby allowing DNA repair. When mutations are numerous, p53 induces apoptosis and avoids the duplication of an injured cell (Albrechtsen et al, 1999).…”

mentioning

confidence: 99%

Detection of mutations within exons 4 to 8 of the p53 tumor suppressor gene in canine mammary glands

Souza¹,

Barros²,

Silva³

et al. 2012

Arq. Bras. Med. Vet. Zootec.

View full text Add to dashboard Cite

Fifteen female canines with mammary tumors and 6 normal females were used to study mutations in exons 4 to 8 of the p53 gene. DNA samples from the tumors, respective adjacent normal mammary tissue and mammary glands from healthy animals were sequenced and analyzed for the presence of mutations. Mutations were found in 71.8% of the samples and the most frequent were missense mutations. The most attacked exons in the mammary tumor were 5, 7 and 8, with 23.4, 31.6 and 23.4% mutations, respectively. Canine mammary tumors are related to mutations in gene p53 and mutations mostly occur in the region of the protein that is linked to the DNA in the cell nucleus, which can change the functionality of the cell and propitiate tumor growth. Despite being macroscopically normal, the mammary tissue adjacent to the tumors has mutations that can lead to recurrence if not removed together with the tumor.

show abstract

Maintenance of genomic integrity by p53: complementary roles for activated and non-activated p53

Cited by 164 publications

References 144 publications

The Human Papillomavirus E6 protein and its contribution to malignant progression

The Human Papillomavirus E6 protein and its contribution to malignant progression

Identification of Tcf-4 as a transcriptional target of p53 signalling

Detection of mutations within exons 4 to 8 of the p53 tumor suppressor gene in canine mammary glands

Contact Info

Product

Resources

About