Results 81 to 90 of about 466,841 (162)

Targeting oncogenic mutant p53 for cancer therapy

open access: yesFrontiers in Oncology, 2015
Among genetic alterations in human cancers, mutations in the tumor suppressor p53 gene are the most common, occurring in over 50% of human cancers. The majority of p53 mutations are missense mutations and result in the accumulation of dysfunctional p53 ...
Tomoo eIwakuma, Alejandro eParrales
doaj   +1 more source

Prediction of progression in pTa and pT1 bladder carcinomas with p53, p16 and pRb. [PDF]

open access: yes, 2004
Currently available prognostic tools appear unable to adequately predict recurrence and progression in non muscle-invasive bladder carcinomas. We aimed to assess the prognostic value of immunohistochemical evaluation of the cell cycle markers p53, p16 ...
S Jordan   +11 more
core   +1 more source

Mouse p53-deficient cancer models as platforms for obtaining genomic predictors of human cancer clinical outcomes [PDF]

open access: yes, 2012
Mutations in the TP53 gene are very common in human cancers, and are associated with poor clinical outcome. Transgenic mouse models lacking the Trp53 gene or that express mutant Trp53 transgenes produce tumours with malignant features in many organs.
Miquel Taron   +64 more
core   +1 more source

Models incorporating chromatin modification data identify functionally important p53 binding sites [PDF]

open access: yes, 2013
Genome-wide prediction of transcription factor binding sites is notoriously difficult. We have developed and applied a logistic regression approach for prediction of binding sites for the p53 transcription factor that incorporates sequence information ...
Barker, Daniel   +2 more
core   +1 more source

DBC1 Regulates p53 Stability via Inhibition of CBP-Dependent p53 Polyubiquitination

open access: yesCell Reports, 2019
Summary: The control of p53 protein stability is critical to its tumor suppressor functions. The CREB binding protein (CBP) transcriptional co-activator co-operates with MDM2 to maintain normally low physiological p53 levels in cells via exclusively ...
Oluwatoyin E. Akande   +6 more
doaj   +1 more source

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  

Upstream Targets in the p53 Pathway

open access: yes, 2013
Small molecule reactivation of mutant forms of the tumour suppressor p53 or wild-type p53 function is an accepted strategy for the development of anticancer therapies.
McCarthy, AR, Lain, S
core   +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

Identification of CNOT1-CCR4-NOT as a suppressor of 53BP1-p53-p21 signaling

open access: yesCell Reports
Summary: Tumor suppressor p53 has inherent propensities to self-associate, which can lead to oncogenic p53 aggregation. The genome caretaker 53BP1 interacts with p53, forms DNA damage-associated condensates, and has been implicated in p53 activation ...
Antonio Galarreta   +5 more
doaj   +1 more source

Nerve Growth Factor Regulation of Transcription Factor p53 Activity

open access: yes, 2007
p53 is recognized as a critical regulator of the cell cycle and apoptosis. Mounting evidence also suggests a role for p53 in the differentiation of several cell types including neuronal precursors. Using the pheochromocytoma PC12 cell model, we studied
Brynczka, Christopher
core  

Home - About - Disclaimer - Privacy