Results 31 to 40 of about 154,391 (307)

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

Protein adduction causes non-mutational inhibition of p53 tumor suppressor

open access: yesCell Reports, 2023
Summary: p53 is a key tumor suppressor that is frequently mutated in human tumors. In this study, we investigated how p53 is regulated in precancerous lesions prior to mutations in the p53 gene.
Ravindran Caspa Gokulan   +10 more
doaj   +1 more source

The multifunctional protein E4F1 links P53 to lipid metabolism in adipocytes

open access: yesNature Communications, 2021
The p53 tumor suppressor is also a regulator of metabolism, but the mechanisms controlling p53-associated metabolic activities remain poorly understood.
Matthieu Lacroix   +22 more
doaj   +1 more source

A New p53 Target Gene, RKIP, Is Essential for DNA Damage-Induced Cellular Senescence and Suppression of ERK Activation

open access: yesNeoplasia: An International Journal for Oncology Research, 2013
p53, a strong tumor suppressor protein, is known to be involved in cellular senescence, particularly premature cellular senescence. Oncogenic stresses, such as Ras activation, can initiate p53-mediated senescence, whereas activation of the Ras-mitogen ...
Su-Jin Lee   +3 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

Molecular basis for modulation of the p53 target selectivity by KLF4

open access: yes, 2012
The tumour suppressor p53 controls transcription of various genes involved in apoptosis, cell-cycle arrest, DNA repair and metabolism. However, its DNA-recognition specificity is not nearly sufficient to explain binding to specific locations in vivo ...
Daniel P. Teufel   +19 more
core   +1 more source

p63 is an alternative p53 repressor in melanoma that confers chemoresistance and a poor prognosis [PDF]

open access: yes, 2013
The role of apoptosis in melanoma pathogenesis and chemoresistance is poorly characterized. Mutations in TP53 occur infrequently, yet the TP53 apoptotic pathway is often abrogated.
Graf, M   +47 more
core   +1 more source

Crosstalk between p53 modifiers at PML bodies

open access: yesMolecular & Cellular Oncology, 2018
Tumor protein p53 (TP53, best known as p53), the most frequently mutated tumor suppressor in cancer, plays a central role in cell fate decisions induced by DNA damage.
Sonja Matt, Thomas G Hofmann
doaj   +1 more source

Multiple C-terminal Lysine residues target p53 for ubiquitin-proteasome-mediated degradation

open access: yes, 2000
This work was supported by the Medical Research Council, the Biotechnology and Biological Research Council, and the Cancer Research Campaign. D.P.L. is a Gibb fellow of the Cancer Research Campaign.In normal cells, p53 is maintained at a low level by ...
Lain, Sonia   +6 more
core   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

Home - About - Disclaimer - Privacy