p53


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p53

A tumor suppressor gene located on the short arm of chromosome 17 that encodes a nucleophosphoprotein that binds DNA and negatively regulates cell division; frequently measured as a marker of malignant diseases.

p53

(pē′fĭf′tē-thrē′)
n.
1. A protein that regulates normal cell growth and proliferation and prevents unrestrained division of cells whose DNA has been damaged, as from ultraviolet or ionizing radiation. The absence of functional p53, usually resulting from a genetic mutation, increases the risk of developing various cancers.
2. The tumor suppressor gene that codes for this protein. Also called TP53.

p53

A 53 kD nuclear phosphoprotein encoded by the proto-oncogene p53, on chromosome 17p13; in its wild form, p53 inhibits cell growth control and transformation; it activates transcription of genes that suppress cell proliferation, acting as a tumor suppressor protein; if p53 is physically lost or functionally inactived, cells can grow without restraint. See Li-Fraumeni syndrome, p21, Tumor suppressor genes, WAF1.

p53

A tumor suppressor gene located on the short arm of chromosome 17 that encodes a nucleophosphoprotein that binds DNA and negatively regulates cell division; frequently measured as a marker of malignant diseases.

p53

A gene that codes for P21. A tumour suppressor gene, the absence or mutation of which can greatly increase the probability that cancer will develop. When DNA damage, as from anticancer drugs, occurs in normal cells the expression of p53 is increased. The p53 protein may then act to protect the cell by halting the cell cycle so that the DNA damage can be repaired, or, if the DNA damage is too severe, p53 protein can kill the cell by APOPTOSIS so that the defective DNA is not passed on. Mutations in p53 have been found in a range of cancers including those of the breast, colon, ovary, bladder and oesophagus. They have also been found to be associated with failure to respond to anticancer drugs.

p53

a tumor suppressor gene active in the cellular response to DNA damage and cell cycle arrest.
References in periodicals archive ?
A low level of p53 induced TWIST2, which kept the MSCs in a stem state, rather than promoting any differentiation.
Elucidating the effects of p53 polymorphisms on cancer risk is a challenging task, especially due to the limited availability of sample cohorts from specific populations.
Depending upon Staining Intensity, p53 Positivity is Graded According to Cheng et al 2013 (9)
Measurement of serum concentration S100B and P53 was performed on eighteen patient samples as described in our previous study.
Primary rabbit polyclonal anti-SIRT1 and p53 (1 : 200 dilution) were incubated with cells for >16 h at 4[degrees]C, and secondary polyclonal rabbit anti-rat immunoglobulin/FITC was added to cells for 1 h at 37[degrees]C.
Following DNA damage, the tumor suppressor protein p53 has a crucial influence on whether cells will survive or die by either stimulating DNA repair or initiating apoptosis if the DNA damage has exceeded a certain threshold.
Active P53 binds to target DNA and determines the choice between triggering cell cycle arrests at a checkpoint to allow DNA repair or activating a special molecular pathway leading to the self-destruction of a cell through apoptosis.
The results (Figure 1A) showed that both mutated and WT p53 proteins were able to bind with this repair protein.
Chi-square test was used (Table 5) to compare frequency of Protein P53 expression in Normal, Dysplastic and Malignant cases.
The 91 positive serum samples of HBsAg were evaluated with respect to the presence of p53 protein using the ELISA method (Bender MedSystem, Vienna, Austria).
Until now, even though ARF was known to be expressed in some tumors with mutated p53, ARF largely was thought to be nonfunctional in this scenario.