Results 61 to 70 of about 2,017,768 (306)

Genome-Wide Analysis of p53 Targets Reveals SCN2A as a Novel Player in p53-Induced Cell Arrest in HPV-Positive Cells

open access: yesViruses
The host transcription factor p53 is a critical tumor suppressor in HPV-induced carcinogenesis, regulating target genes involved in cell cycle arrest and apoptosis. However, the p53 targets have not been thoroughly analyzed in HPV-infected cells. In this
Yudi Zhang   +4 more
doaj   +1 more source

Long noncoding RNAs: p53's secret weapon in the fight against cancer?

open access: yesPLoS Biology, 2019
p53 regulates the expression of hundreds of genes. Recent surprising observations indicate that no single protein-coding gene controls the tumor suppressor effects of p53.
Emily Dangelmaier   +2 more
doaj   +1 more source

Selective inhibition of microRNA accessibility by RBM38 is required for p53 activity [PDF]

open access: yes, 2011
MicroRNAs (miRNAs) interact with 3'-untranslated regions of messenger RNAs to restrict expression of most protein-coding genes during normal development and cancer. RNA-binding proteins (RBPs) can control the biogenesis, stability and activity of miRNAs.
Horlings, HM   +41 more
core   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

open access: yesMolecular Oncology, EarlyView.
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

Hdm2 recruits a hypoxia-sensitive corepressor to negatively regulate p53-dependent transcription [PDF]

open access: yes, 2003
The transcription factor p53 lies at the center of a protein network that controls cell cycle progression and commitment to apoptosis. p53 is inactive in proliferating cells, largely because of negative regulation by the Hdm2/Mdm2 oncoprotein, with which
Darley, Matthew   +11 more
core   +1 more source

MITF maintains genome stability in nonmelanocyte lineages

open access: yesMolecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir   +13 more
wiley   +1 more source

Mutations of the p53 gene in lymphoid leukemia [PDF]

open access: yesBlood, 1991
p53 is currently considered to be a tumor suppressor gene product, and its alterations are suggested to be involved in several human malignancies. Here we show evidence of the possible involvement of p53 gene mutations in lymphoid leukemias studied by reverse transcriptase- polymerase chain reaction, single strand conformation polymorphism analysis ...
F.Takaku   +7 more
openaire   +3 more sources

Distinct promoter elements mediate the co-operative effect of Brn-3a and p53 on the p21 promoter and their antagonism on the Bax promoter [PDF]

open access: yes, 2002
Although the promoters of both the Bax and p21 genes are activated by p53, they differ in the effect on this activation of the POU family transcription factor Brn-3a. Thus, Brn-3a inhibits activation of the Bax promoter by p53 but enhances the ability of
Budhram-Mahadeo, VS   +2 more
core  

FAK deletion promotes p53-mediated induction of p21, DNA-damage responses and radio-resistance in advanced squamous cancer cells [PDF]

open access: yes, 2011
Focal adhesion kinase (FAK) is a cytoplasmic tyrosine kinase that is elevated in a variety of human cancers. While FAK is implicated in many cellular processes that are perturbed in cancer, including proliferation, actin and adhesion dynamics ...
Moran-Jones Kim   +22 more
core   +1 more source

A novel quinazolinone insulin receptor inhibitor and its synergy with an EGFR inhibitor in glucose‐driven glioblastoma

open access: yesMolecular Oncology, EarlyView.
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka   +9 more
wiley   +1 more source

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