Results 41 to 50 of about 342,417 (266)
Many therapeutic antibodies are humanized from animal sources. In the humanization process, complementarity determining region grafting is tedious and highly prone to failure.
Wei-Li Ling +6 more
doaj +1 more source
A High-Throughput Cell-Based Screen Identified a 2-[(E)-2-Phenylvinyl]-8-Quinolinol Core Structure That Activates p53. [PDF]
p53 function is frequently inhibited in cancer either through mutations or by increased degradation via MDM2 and/or E6AP E3-ubiquitin ligases. Most agents that restore p53 expression act by binding MDM2 or E6AP to prevent p53 degradation.
John Bechill +4 more
doaj +1 more source
Development of DNA aptamer screens that are both simple and informative can increase the success rate of DNA aptamer selection and induce greater adoption.
Wei Mei Guo +6 more
doaj +1 more source
p53 α-Helix mimetics antagonize p53/MDM2 interaction and activate p53 [PDF]
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
openaire +2 more sources
Macroautophagy (autophagy hereafter) captures, degrades, and recycles intracellular components to maintain metabolic homeostasis and protein and organelle quality control. Autophagy thereby promotes survival in starvation and prevents tissue degeneration. There is an important relationship between autophagy and p53.
openaire +2 more sources
Tumor suppressor protein p53 (TP53) is a key transcription factor that, in response to various stress signals, regulates numerous genes involved in a broad range of cellular functions including DNA repair, apoptosis, cell cycle arrest, senescence, metabolism, etc [...]
openaire +4 more sources
A long-term goal in the cancer-field has been to develop strategies for treating p53-mutated tumors. A novel small-molecule, PG3-Oc, restores p53 pathway-signaling in tumor cells with mutant-p53, independently of p53/p73. PG3-Oc partially upregulates the
Xiaobing Tian +7 more
doaj +1 more source
The ubiquitin‐proteasome system and autophagy as guardians of the cellular proteome
This Perspective covers the three principles governing the crosstalk between the ubiquitin‐proteasome system and autophagy in cellular proteostasis: (1) a shared ubiquitin code routing substrates via shuttle factors or autophagy receptors; (2) spatial compartmentalization into phase‐separated degradation hubs and organelle‐specific modules (exemplified
Ivan Dikic
wiley +1 more source
Insulin receptor tyrosine kinase substrate enhances low levels of MDM2-mediated p53 ubiquitination. [PDF]
The tumor suppressor p53 controls multiple cellular functions including DNA repair, cell cycle arrest and apoptosis. MDM2-mediated p53 ubiquitination affects both degradation and cytoplasmic localization of p53.
Ke-Sheng Wang +8 more
doaj +1 more source
MDM2 is the principal inhibitor of p53, and MDM2 inhibitors can disrupt the physical interaction between MDM2 and p53. The half-life of p53 is very short in normal cells and tissues, and an uncontrolled increase in p53 levels has potential harmful ...
Arianna Romani +5 more
doaj +1 more source

