p63-related signaling at a glance.

J Cell Sci

Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, 11724, USA

Published: September 2020

p63 (also known as TP63) is a transcription factor of the p53 family, along with p73. Multiple isoforms of p63 have been discovered and these have diverse functions encompassing a wide array of cell biology. p63 isoforms are implicated in lineage specification, proliferative potential, differentiation, cell death and survival, DNA damage response and metabolism. Furthermore, p63 is linked to human disease states including cancer. p63 is critical to many aspects of cell signaling, and in this Cell science at a glance article and the accompanying poster, we focus on the signaling cascades regulating TAp63 and ΔNp63 isoforms and those that are regulated by TAp63 and ΔNp63, as well the role of p63 in disease.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7502597PMC
http://dx.doi.org/10.1242/jcs.228015DOI Listing

Publication Analysis

Top Keywords

tap63 Δnp63
8
p63
6
p63-related signaling
4
signaling glance
4
glance p63
4
p63 tp63
4
tp63 transcription
4
transcription factor
4
factor p53
4
p53 family
4

Similar Publications

Immature oocytes enclosed in primordial follicles stored in female ovaries are under constant threat of DNA damage induced by endogenous and exogenous factors. Checkpoint kinase 2 (CHEK2) is a key mediator of the DNA damage response (DDR) in all cells. Genetic studies have shown that CHEK2 and its downstream targets, p53, and TAp63, regulate primordial follicle elimination in response to DNA damage.

View Article and Find Full Text PDF

Activating transcription factor 3 mediates apoptosis and cell cycle arrest in TP53-mutated anaplastic thyroid cancer cells.

Thyroid Res

August 2024

Division of Medical Biotechnology, Department of Medical Laboratory Sciences, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.

Background: It is believed that loss of p53 function plays a crucial role in the progression of well to poorly differentiated thyroid cancers including anaplastic thyroid carcinoma (ATC). Given the poor prognosis of ATC due to its strong therapeutic resistance, there is a need to establish new therapeutic targets to extend the survival of ATC patients. Activating transcription factor 3 (ATF3) can inhibit the oncogenic activity of mutant p53 and, as a result, contribute to tumor suppression in several TP53-mutated cancers.

View Article and Find Full Text PDF

Inhibition of hepatic p63 ameliorates steatohepatitis with fibrosis in mice.

Mol Metab

July 2024

Department of Physiology, CIMUS, University of Santiago de Compostela, Santiago de Compostela, 15782, Spain; CIBER Fisiopatologia de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, 15782, Spain; Galicia Agency of Innovation (GAIN), Xunta de Galicia, Santiago de Compostela, 15702, Spain. Electronic address:

Objective: p63 is a transcription factor involved in multiple biological functions. In the liver, the TAp63 isoform induces lipid accumulation in hepatocytes. However, the role of liver TAp63 in the progression of metabolic dysfunction-associated steatohepatitis (MASH) with fibrosis is unknown.

View Article and Find Full Text PDF
Article Synopsis
  • TGFβ plays a significant role in inflammation, wound healing, and cancer, acting as a tumor suppressor in squamous cell carcinoma (SCC), which is linked to high ΔNp63 levels.
  • Research shows that TGFβ selectively increases ΔNp63 protein in healthy cells via canonical signaling, but the relationship between mRNA levels and protein is complicated, showing initial increases followed by later declines.
  • The interactions between TGFβ and p63 may affect epithelial-to-mesenchymal transition and influence tumor behavior and treatment responses in SCC.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!