Results 41 to 50 of about 430,765 (317)

SIRT1 Undergoes Alternative Splicing in a Novel Auto-Regulatory Loop with p53 [PDF]

open access: yes, 2010
Background The NAD-dependent deacetylase SIRT1 is a nutrient-sensitive coordinator of stress-tolerance, multiple homeostatic processes and healthspan, while p53 is a stress-responsive transcription factor and our paramount tumour suppressor. Thus, SIRT1-
Ahmed, Shafiq U.   +41 more
core   +1 more source

Identification and Characterization of an eIF4e DNA Aptamer That Inhibits Proliferation With High Throughput Sequencing

open access: yesMolecular Therapy: Nucleic Acids, 2014
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 and Atherosclerosis [PDF]

open access: yesCirculation Research, 2001
Subendothelial macrophages are a major cellular component of atherosclerotic lesions. In response to subendothelial retention of modified lipoproteins,1 2 blood-borne monocytes enter the subendothelial space, differentiate into macrophages, and accumulate large amounts of lipoprotein-derived cholesterol (foam cells).3 4 Specific consequences of ...
openaire   +2 more sources

The degradation of p53 and its major E3 ligase Mdm2 is differentially dependent on the proteasomal ubiquitin receptor S5a. [PDF]

open access: yes, 2014
p53 and its major E3 ligase Mdm2 are both ubiquitinated and targeted to the proteasome for degradation. Despite the importance of this in regulating the p53 pathway, little is known about the mechanisms of proteasomal recognition of ubiquitinated p53 and
J Das   +11 more
core   +1 more source

Autophagy and p53 [PDF]

open access: yesCold Spring Harbor Perspectives in Medicine, 2016
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

p53 α-Helix mimetics antagonize p53/MDM2 interaction and activate p53 [PDF]

open access: yesMolecular 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
openaire   +2 more sources

Inactivation and inducible oncogenic mutation of p53 in gene targeted pigs. [PDF]

open access: yes, 2012
Mutation of the tumor suppressor p53 plays a major role in human carcinogenesis. Here we describe gene-targeted porcine mesenchymal stem cells (MSCs) and live pigs carrying a latent TP53(R167H) mutant allele, orthologous to oncogenic human mutant TP53 ...
Eckhard Wolf   +41 more
core   +1 more source

P53-independent partial restoration of the p53 pathway in tumors with mutated p53 through ATF4 transcriptional modulation by ERK1/2 and CDK9

open access: yesNeoplasia: An International Journal for Oncology Research, 2021
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

Recent Advances in p53 [PDF]

open access: yesBiomolecules, 2021
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

Independent regulation of P53 stabilisation and activation after Rb deletion in primary epithelial cells [PDF]

open access: yes, 2010
We have previously reported that deletion of the retinoblastoma gene Rb leads to rapid but transient p53 stabilisation. We investigated here the pathways involved.
Bellamy, Christopher   +4 more
core   +1 more source

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