Results 21 to 30 of about 646,683 (270)
p53 α-Helix mimetics antagonize p53/MDM2 interaction and activate p53 [PDF]
Molecular Cancer Therapeutics, 2005 Abstract Overexpression or hyperactivation of MDM2 contributes to functional inactivation of wild-type p53 in nearly 50% of tumors. Inhibition of p53 by MDM2 depends on binding between an NH2-terminal (residues 16–28) p53 α-helical peptide and a hydrophobic pocket on MDM2, presenting an attractive target for development of inhibitors ...
Lihong, Chen +5 more
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Frontiers in Oncology, 2021 BackgroundWe conducted an analysis of previous adenoviral p53 (Ad-p53) treatment data in recurrent head and neck squamous cell carcinoma (HNSCC) patients to identify optimal Ad-p53 treatment methods for future clinical trials.MethodsThe analysis involved
Robert E. Sobol +6 more
doaj +1 more source
p53 isoforms change p53 paradigm [PDF]
Molecular & Cellular Oncology, 2014 Although p53 defines cellular responses to cancer treatment it is not clear how p53 can be used to control cell fate outcome. Data demonstrate that so-called p53 does not exist as a single protein, but is in fact a group of p53 protein isoforms whose expression can be manipulated to control the cellular response to treatment.
openaire +3 more sources
p53 isoforms can regulate p53 transcriptional activity [PDF]
Genes & Development, 2005 The recently discovered p53-related genes, p73 and p63, express multiple splice variants and N-terminally truncated forms initiated from an alternative promoter in intron 3. To date, no alternative promoter and multiple splice variants have been described for the p53 gene.
Bourdon, J C +7 more
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Tumor-Targeted Delivery of the p53-Activating Peptide VIP116 with PEG-Stabilized Lipodisks
Nanomaterials, 2020 Stapled peptides targeting the interaction between p53 and its negative regulators MDM2 and MDM4 have exhibited great potential as anti-cancer drugs, albeit with room for improvement in formulation and tumor specificity.
Sara Lundsten +7 more
doaj +1 more source
Mutant p53 establishes targetable tumor dependency by promoting unscheduled replication [PDF]
, 2017 Gain-of-function (GOF) p53 mutations are observed frequently in most intractable human cancers and establish dependency for tumor maintenance and progression.
Beckerman +14 more
core +2 more sources
USP11 regulates p53 stability by deubiquitinating p53 [PDF]
Journal of Zhejiang University SCIENCE B, 2014 The p53 tumor suppressor protein coordinates the cellular responses to a broad range of cellular stresses, leading to DNA repair, cell cycle arrest or apoptosis. The stability of p53 is essential for its tumor suppressor function, which is tightly controlled by ubiquitin-dependent degradation primarily through its negative regulator murine double ...
Jia-ying, Ke +7 more
openaire +2 more sources
Monitoring flux in signalling pathways through measurements of 4EBP1-mediated eIF4F complex assembly
BMC Biology, 2019 Background The most commonly occurring cancer mutations, including oncogenes such as MYC, Ras and PIK3C, are found in signal transductions pathways feeding into the translational machinery.
Yuri Frosi +4 more
doaj +1 more source
The Basally Expressed p53-Mediated Homeostatic Function
Frontiers 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
DIMP53-1:A novel small-molecule dual inhibitor of p53-MDM2/X interactions with multifunctional p53-dependent anticancer properties [PDF]
, 2017 The transcription factor p53 plays a crucial role in cancer development and dissemination, and thus, p53-targeted therapies are among the most encouraging anticancer strategies.
Baeriswyl +23 more
core +2 more sources