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/PMC7502597 | PMC |
http://dx.doi.org/10.1242/jcs.228015 | DOI Listing |
Dev Biol
January 2025
The Jackson Laboratory, 600 Main Street, Bar Harbor, ME, 04609, USA. Electronic address:
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 PDFThyroid 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 PDFNature
August 2024
Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas, USA.
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 PDFSci Rep
March 2024
Research Center of Applied Molecular Oncology (RECAMO), Masaryk Memorial Cancer Institute, Zluty Kopec 7, 656 53, Brno, Czech Republic.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!