Results 71 to 80 of about 154,391 (307)
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska +13 more
wiley +1 more source
Tumor Suppressor Protein p53 Regulates Megakaryocytic Polyploidization and Apoptosis [PDF]
The molecular mechanisms underlying differentiation of hematopoietic stem cells into megakaryocytes are poorly understood. Tumor suppressor protein p53 can act as a transcription factor affecting both cell cycle control and apoptosis, and we have previously shown that p53 is activated during terminal megakaryocytic (Mk) differentiation of the CHRF-288 ...
Peter G, Fuhrken +4 more
openaire +2 more sources
Breast Cancer Therapy by Small-Molecule Reactivation of Mutant p53
Tumor suppressor p53 is essential for maintaining DNA stability and preventing cancer. Under normal conditions, the p53 protein is either degraded or bound to a negative regulator, rendering it inactive, but when DNA damage occurs, p53 is activated ...
Simon H. Slight, Salman M. Hyder
doaj +1 more source
SIRT1 Undergoes Alternative Splicing in a Novel Auto-Regulatory Loop with p53
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
Quantitative model for inferring dynamic regulation of the tumour suppressor gene p53 [PDF]
Background: The availability of various "omics" datasets creates a prospect of performing the study of genome-wide genetic regulatory networks. However, one of the major challenges of using mathematical models to infer genetic regulation from microarray ...
Junbai Wang +7 more
core +1 more source
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source
The regulation of the function of the tumor suppressor protein p53 [PDF]
AbstractTerms to be familiar with before you start to solve the test: Tumor suppressor proteins; p53 protein; p53‐positive and p53‐negative tumors; transcription factors; protein phosphorylation; retinoblastoma protein; Go phase; apoptosis; chaperone; transfection; expression plasmid; cDNA; papillomavirus; Western blot analysis; γ‐irradiation; mitotic ...
openaire +1 more source
Crosstalk between c-Jun and TAp73alpha/beta contributes to the apoptosis–survival balance [PDF]
The p53-family member p73 plays a role in various cellular signaling pathways during development and growth control and it can have tumor suppressor properties. Several isoforms of p73 exist with considerable differences in their function.
Simon J. van Heeringen +23 more
core +1 more source
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober +16 more
wiley +1 more source
Proteins of the S100 family regulate the oligomerization of p53 tumor suppressor [PDF]
S100B protein is elevated in the brains of patients with early stages of Alzheimer's disease and Down's syndrome. S100A4 is correlated with the development of metastasis. Both proteins bind to p53 tumor suppressor. We found that both S100B and S100A4 bind to the tetramerization domain of p53 (residues 325-355) only when exposed in lower oligomerization
Fernández-Fernández, María Rosario +2 more
openaire +3 more sources

