Results 21 to 30 of about 430,765 (317)

The Basally Expressed p53-Mediated Homeostatic Function

open access: yesFrontiers in Cell and Developmental Biology, 2021
Apart from mutations in the p53 gene, p53 functions can be alternatively compromised by a decrease in nuclear p53 protein levels or activities. In accordance, enhanced p53 protein turnover due to elevated expression of the critical p53 E3 ligase MDM2 or ...
Isha Nagpal, Zhi-Min Yuan
doaj   +1 more source

Molecular basis for modulation of the p53 target selectivity by KLF4 [PDF]

open access: yes, 2012
The tumour suppressor p53 controls transcription of various genes involved in apoptosis, cell-cycle arrest, DNA repair and metabolism. However, its DNA-recognition specificity is not nearly sufficient to explain binding to specific locations in vivo ...
Daniel P. Teufel   +19 more
core   +1 more source

Point mutations of the P53 gene, human hepatocellular carcinoma and aflatoxins [PDF]

open access: yes, 1993
The tumor suppressor p53 exerts important protective functions towards DNA-damaging agents. Its inactivation by allelic deletions or point mutations within the P53 gene as well as complex formation of wildtype p53 with cellular or viral proteins is a ...
Caselmann, Wolfgang H.   +1 more
core   +1 more source

The Enigma of p53 [PDF]

open access: yesCold Spring Harbor Symposia on Quantitative Biology, 2016
This perspective will focus on the physiological impact of wild-type and mutant p53 activities. In particular, the tissue-specific nature of activation of p53 targets and their subsequent effects on cell behavior will be discussed. Because mutations in p53 are common in human cancers, the regulation and physiological consequences of mutant p53 proteins
openaire   +2 more sources

A p53-independent role for the MDM2 antagonist Nutlin-3 in DNA damage response initiation. [PDF]

open access: yes, 2011
BACKGROUND: The mammalian DNA-damage response (DDR) has evolved to protect genome stability and maximize cell survival following DNA-damage. One of the key regulators of the DDR is p53, itself tightly regulated by MDM2. Following double-strand DNA breaks
Valentine, Jane M.   +11 more
core   +1 more source

A yeast two-hybrid system for the screening and characterization of small-molecule inhibitors of protein–protein interactions identifies a novel putative Mdm2-binding site in p53

open access: yesBMC Biology, 2017
Background Protein–protein interactions (PPIs) are fundamental to the growth and survival of cells and serve as excellent targets to develop inhibitors of biological processes such as host-pathogen interactions and cancer cell proliferation.
Jin Huei Wong   +6 more
doaj   +1 more source

Identification of Small Molecules that Modulate Mutant p53 Condensation

open access: yesiScience, 2020
Summary: Structural mutants of p53 induce global p53 protein destabilization and misfolding, followed by p53 protein aggregation. First evidence indicates that p53 can be part of protein condensates and that p53 aggregation potentially transitions ...
Clara Lemos   +21 more
doaj   +1 more source

PINTing for p53 [PDF]

open access: yesGenome Biology, 2013
A new study identifies the long noncoding RNA Pintas a regulator of cellular proliferation and a target of the p53 pathway.
openaire   +2 more sources

The p53 pathway [PDF]

open access: yesThe Journal of Pathology, 1999
Abnormalities of the p53 tumour suppressor gene are among the most frequent molecular events in human and animal neoplasia. Moreover, p53 is one of the most studied proteins in the whole of contemporary biology, with more than 12,500 papers so far written!
C, Prives, P A, Hall
openaire   +2 more sources

p53 Expression in Colorectal Carcinoma in Relation to Histopathological Features in Ugandan Patients. [PDF]

open access: yes, 2008
It has been shown that colorectal carcinoma is increasing in incidence in African countries. This could be due to change in life style. Molecular pathogenesis of colorectal cancer commonly involves mutation in p53 gene which leads to expression of p53 ...
Rambau, PF   +6 more
core   +1 more source

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