p53 directly regulates the glycosidase FUCA1 to promote chemotherapy-induced cell death [PDF]
p53 is a central factor in tumor suppression as exemplified by its frequent loss in human cancer. p53 exerts its tumor suppressive effects in multiple ways, but the ability to invoke the eradication of damaged cells by programmed cell death is considered
Baudot, Alice D. +5 more
core +2 more sources
Zn(II)-curc targets p53 in thyroid cancer cells [PDF]
P53 mutation is a common event in many cancers, including thyroid carcinoma. Defective p53 activity promotes cancer resistance to therapies and a more malignant phenotype, acquiring oncogenic functions.
Crispini, Alessandra +3 more
core +2 more sources
Prediction Of Cancer Possibility By Pattern Recognition And Statistical Study Of Expression Of Gene Level Of Cancer Cells [PDF]
The activity of the p53 tumor-suppressor protein has a key role in controlling both cancer and aging: under activity encourages the growth of cancer, and over activity can accelerate the aging process.
Devang Odedra, Medhavi Mallick
core +2 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
Identification of LDH-A as a therapeutic target for cancer cell killing via (i) p53/NAD(H)-dependent and (ii) p53 independent pathways [PDF]
Most cancer cells use aerobic glycolysis to fuel their growth. The enzyme lactate dehydrogenase-A (LDH-A) is key to cancer’s glycolytic phenotype, catalysing the regeneration of nicotinamide adenine dinucleotide (NAD þ ) from reduced nicotinamide adenine
Allison, Simon J. +6 more
core +1 more source
Hematopoietic (stem) cells—The elixir of life?
The aging of HSCs (hematopoietic stem cells) and the blood system leads to the decline of other organs. Rejuvenating aged HSCs improves the function of the blood system, slowing the aging of the heart, kidney, brain, and liver, and the occurrence of age‐related diseases.
Emilie L. Cerezo +4 more
wiley +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
Disordered but rhythmic—the role of intrinsic protein disorder in eukaryotic circadian timing
Unstructured domains known as intrinsically disordered regions (IDRs) are present in nearly every part of the eukaryotic core circadian oscillator. IDRs enable many diverse inter‐ and intramolecular interactions that support clock function. IDR conformations are highly tunable by post‐translational modifications and environmental conditions, which ...
Emery T. Usher, Jacqueline F. Pelham
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
Scotin, a novel p53-inducible proapoptotic protein located in the ER and the nuclear membrane [PDF]
p53 is a transcription factor that induces growth arrest or apoptosis in response to cellular stress. To identify new p53-inducible proapoptotic genes, we compared, by differential display, the expression of genes in spleen or thymus of normal and p53 ...
Bourdon, J.-C. +4 more
core +5 more sources

