The mice) that is lacking the N-terminal transactivation domain,

The “p14/19 ARF” positive feedback loop is chosen from the paper entitled extbf{The p53 pathway: positive and negative feedback loops} cite{PL}. The p53-pathway has an important role in tumor surveillance mechanism that responds to oncogenic stimuli by inducing apoptosis or cell cycle arrest. Inactivation of this gene is an important step in carcinogenesis. Different external factors such as stress cause unique post-translational modifications on p53 that lead different kinds of  responses for cell fate decisions.

p53 is a hub protein that regulates/is regulated by many other signal transduction pathways, which all have an important role in tumorigenesis. Since this is the case, many positive and negative feedback loops exist within the pathway, which the paper explains in detail, but I will focus on one of the presented positive feedback loops named extbf{SIAH-1/$eta$-catenin/p14/19 ARF loop}.The activation of p53 can be caused by different number of oncogenes (E2F-1, $eta$-catenin, RAS, MYC are reported in the article) and is carried out by a positive feedback loop that results in the production of p19/14 ARF, which then inhibits MDM-2 (a ubiquitin ligase that functions as a negative regulator for p53) leading to an increased level of p53. In detail, when p53 is active, it positively regulates the transcription of SIAH-1 (a ubiquitin ligase). This inhibits $eta$-catenin. It is stated that $eta$-catenin regulates p14/19 ARF gene, which in response inhibits MDM-2, resulting in an increase of p53 levels. This behavior is creating a positive feedback loop.

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The authors conclude that SIAH-1 has an important role in connecting the “Wnt-$eta$-catenin-APC pathway” with p53 pathway.For this question, I wanted to review the paper entitled extbf{“Human $Delta$Np73 regulates a dominant negative feedback loop for TAp73 and p53“} cite{NL}. The authors, based on the experimental results, claim that human p73 $Delta$N isoform ($Delta$Np73 initially reported in mice) that is lacking the N-terminal transactivation domain, is acting as dominant negative regulator of p53 and has potential role in carcinogenesis. The model shown in their paper is validated by a series of experiments, all supporting that $Delta$Np73 regulates TAp73 (TA counterpart of $Delta$Np73) and p53 function, along with tightly regulating its own expression.