scholarly journals Mutant p53 protein, master regulator of human malignancies: a report on the fifth Mutant p53 Workshop

2011 ◽  
Vol 19 (1) ◽  
pp. 180-183 ◽  
Author(s):  
G Blandino ◽  
W Deppert ◽  
P Hainaut ◽  
A Levine ◽  
G Lozano ◽  
...  
Keyword(s):  
P53 Protein ◽  
Mutant P53 ◽  
Master Regulator

Human p53 and CDC2Hs genes combine to inhibit the proliferation of Saccharomyces cerevisiae

1992 ◽  
Vol 12 (3) ◽  
pp. 1357-1365
Author(s):  
J M Nigro ◽  
R Sikorski ◽  
S I Reed ◽  
B Vogelstein
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Growth Inhibition ◽  
Mammalian Cells ◽  
P53 Protein ◽  
Inducible Promoter ◽  
Mutant P53 ◽  
Wild Type ◽  
Growth Inhibitory Activity ◽  
Wild Type P53 ◽  
P53 Genes

Human wild-type and mutant p53 genes were expressed under the control of a galactose-inducible promoter in Saccharomyces cerevisiae. The growth rate of the yeast was reduced in cells expressing wild-type p53, whereas cells transformed with mutant p53 genes derived from human tumors were less affected. Coexpression of the normal p53 protein with the human cell cycle-regulated protein kinase CDC2Hs resulted in much more pronounced growth inhibition that for p53 alone. Cells expressing p53 and CDC2Hs were partially arrested in G1, as determined by morphological analysis and flow cytometry. p53 was phosphorylated when expressed in the yeast, but differences in phosphorylation did not explain the growth inhibition attributable to coexpression of p53 and CDC2Hs. These results suggest that wild-type p53 has a growth-inhibitory activity in S. cerevisiae similar to that observed in mammalian cells and suggests that this yeast may provide a useful model for defining the pathways through which p53 acts.

Analysis of mutant P53 protein in osteosarcomas and other malignant and benign lesions of bone

1993 ◽  
Vol 119 (3) ◽  
pp. 172-178 ◽  
Author(s):  
Yoshimichi Ueda ◽  
Barbara Dockhorn-Dworniczak ◽  
Sebastian Blasius ◽  
Walter Mellin ◽  
Paul Wuisman ◽  
...  
Keyword(s):  
P53 Protein ◽  
Mutant P53 ◽  
Benign Lesions

scholarly journals ErbB2 inhibition by lapatinib promotes degradation of mutant p53 protein in cancer cells

Oncotarget ◽  
2016 ◽  
Vol 8 (4) ◽  
pp. 5823-5833 ◽  
Author(s):  
Dun Li ◽  
Natalia D. Marchenko
Keyword(s):  
Cancer Cells ◽  
P53 Protein ◽  
Mutant P53

Mutant p53 protein associated with chemosensitivity in breast cancer specimens

The Lancet ◽  
1994 ◽  
Vol 344 (8937) ◽  
pp. 1647-1648 ◽  
Author(s):  
OssiR. Koechli ◽  
GabrielN. Schaer ◽  
Burkhart Seifert ◽  
René Hornung ◽  
Urs Haller ◽  
...  
Keyword(s):  
Breast Cancer ◽  
P53 Protein ◽  
Mutant P53

Immunohistochemical expression of the mutant p53 protein and nuclear DNA content during the transition from benign to malignant breast disease

1994 ◽  
Vol 25 (11) ◽  
pp. 1228-1233 ◽  
Author(s):  
Elina T. Eriksson ◽  
Hendrik Schimmelpenning ◽  
Ulla Aspenblad ◽  
Anders Zetterberg ◽  
Gert U. Auer
Keyword(s):  
Dna Content ◽  
Nuclear Dna ◽  
P53 Protein ◽  
Nuclear Dna Content ◽  
Breast Disease ◽  
Mutant P53 ◽  
Immunohistochemical Expression ◽  
Malignant Breast

scholarly journals PO-0612: Significance of co-expression of mutant p53 protein and Ki67 in locally advanced HNSCC post chemo-RT

2017 ◽  
Vol 123 ◽  
pp. S319
Author(s):  
P. Baskaran Shanmuga ◽  
K. Periasamy ◽  
S. Sharma ◽  
G.K. Singh ◽  
V. Yadav ◽  
...  
Keyword(s):  
P53 Protein ◽  
Locally Advanced ◽  
Mutant P53

scholarly journals The mdm-2 oncogene can overcome wild-type p53 suppression of transformed cell growth

1993 ◽  
Vol 13 (1) ◽  
pp. 301-306 ◽  
Author(s):  
C A Finlay
Keyword(s):  
P53 Protein ◽  
Mutant P53 ◽  
Wild Type ◽  
Rat Embryo ◽  
Ras Gene ◽  
Double Minute ◽  
Murine Double Minute ◽  
Low Levels ◽  
Wild Type P53 ◽  
P53 Genes

Expression of a p53-associated protein, Mdm-2 (murine double minute-2), can inhibit p53-mediated transactivation. In this study, overexpression of the Mdm-2 protein was found to result in the immortalization of primary rat embryo fibroblasts (REFs) and, in conjunction with an activated ras gene, in the transformation of REFs. The effect of wild-type p53 on the transforming properties of mdm-2 was determined by transfecting REFs with ras, mdm-2, and normal p53 genes. Transfection with ras plus mdm-2 plus wild-type p53 resulted in a 50% reduction in the number of transformed foci (relative to the level for ras plus mdm-2); however, more than half (9 of 17) of the cell lines derived from these foci expressed low levels of a murine p53 protein with the characteristics of a wild-type p53. These results are in contrast to previous studies which demonstrated that even minimal levels of wild-type p53 are not tolerated in cells transformed by ras plus myc, E1A, or mutant p53. The mdm-2 oncogene can overcome the previously demonstrated growth-suppressive properties of p53.

scholarly journals TRRAP is essential for regulating the accumulation of mutant and wild-type p53 in lymphoma

Blood ◽  
2018 ◽  
Vol 131 (25) ◽  
pp. 2789-2802 ◽  
Author(s):  
Alexander Jethwa ◽  
Mikołaj Słabicki ◽  
Jennifer Hüllein ◽  
Marius Jentzsch ◽  
Vineet Dalal ◽  
...  
Keyword(s):  
Protein Stability ◽  
P53 Protein ◽  
Mutant P53 ◽  
Wild Type ◽  
Therapeutic Targeting ◽  
Key Points ◽  
Wild Type P53

Key Points The HAT complex member TRRAP is vital for maintaining high p53 levels by shielding it against the natural p53 degradation machinery. Acetylation-modifying complexes regulate p53 protein stability, which may provide a basis for therapeutic targeting of mutant p53.

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