Results 41 to 50 of about 653,143 (286)

The Expression Levels of XLF and Mutant P53 Are Inversely Correlated in Head and Neck Cancer Cells. [PDF]

open access: yes, 2016
XRCC4-like factor (XLF), also known as Cernunnos, is a protein encoded by the human NHEJ1 gene and an important repair factor for DNA double-strand breaks.
Chen, Wei   +8 more
core   +2 more sources

MDM2 inhibitors-mediated disruption of mitochondrial metabolism: A novel therapeutic strategy for retinoblastoma

open access: yesFrontiers in Oncology, 2022
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

Hyperglycemia triggers HIPK2 protein degradation [PDF]

open access: yes, 2016
Homeodomain interacting protein kinase-2 (HIPK2) is an evolutionary conserved kinase that modulates several key molecular pathways to restrain tumor growth and induce p53-depending apoptotic cell-death in response to anticancer therapies. HIPK2 silencing
Baldari, Silvia   +6 more
core   +2 more sources

OTUD5 Regulates p53 Stability by Deubiquitinating p53

open access: yesPLoS ONE, 2013
The p53 tumour suppressor protein is a transcription factor that prevents oncogenic progression by activating the expression of apoptosis and cell-cycle arrest genes in stressed cells. The stability of p53 is tightly regulated by ubiquitin-dependent degradation, driven mainly by its negative regulators ubiquitin ligase MDM2.In this study, we have ...
Judong Luo   +7 more
openaire   +4 more sources

Prediction Of Cancer Possibility By Pattern Recognition And Statistical Study Of Expression Of Gene Level Of Cancer Cells [PDF]

open access: yes, 2011
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

P53

open access: yesEuropean Journal of Cancer Supplements, 2015
This study used data from population-based cancer registries and total mortality over the past quarter of a century in NIITPM, Novosibirsk. The follow-up period was from 1985 to 2014. Both registers operated in the two regions, the most typical for the city. The results can be extrapolated to the entire population of Novosibirsk. For long-term analysis
S. Kurilovich   +2 more
openaire   +3 more sources

p53 restoration in small cell lung cancer identifies a latent cyclophilin-dependent necrosis mechanism

open access: yesNature Communications, 2023
The p53 tumor suppressor regulates multiple context-dependent tumor suppressive programs. Although p53 is mutated in ~90% of small cell lung cancer (SCLC) tumors, how p53 mediates tumor suppression in this context is unknown. Here, using a mouse model of
Jonuelle Acosta   +18 more
doaj   +1 more source

The human adenovirus 5 L4 promoter is activated by cellular stress response protein p53 [PDF]

open access: yes, 2013
During adenovirus infection, the emphasis of gene expression switches from early genes to late genes in a highly regulated manner. Two gene products, L4-22K and L4-33K, contribute to this switch by activating the Major Late Transcription Unit (MLTU) and ...
Leppard, Keith, Wright, Jordan
core   +1 more source

Organoids in pediatric cancer research

open access: yesFEBS Letters, EarlyView.
Organoid technology has revolutionized cancer research, yet its application in pediatric oncology remains limited. Recent advances have enabled the development of pediatric tumor organoids, offering new insights into disease biology, treatment response, and interactions with the tumor microenvironment.
Carla RĂ­os Arceo, Jarno Drost
wiley   +1 more source

Oncogenic Gain of Function in Glioblastoma Is Linked to Mutant p53 Amyloid Oligomers. [PDF]

open access: yes, 2020
Tumor-associated p53 mutations endow cells with malignant phenotypes, including chemoresistance. Amyloid-like oligomers of mutant p53 transform this tumor suppressor into an oncogene.
de Oliveira, Guilherme AP   +8 more
core   +1 more source

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