Track topics on Twitter Track topics that are important to you
The global transcription factor, p53, is a master regulator of gene expression in cells. Mutations in the TP53 gene promote unregulated cell growth through the inactivation of downstream effectors of the p53 pathway. In fact, mutant p53 is highly prone to misfolding and frequently resides inside the cell as large aggregates, causing loss of physiological function of the tumor-suppressor protein. Here, we review the plausible reasons for functional loss of p53 including amyloid formation leading to unhindered cancer progression. We discuss previous as well as recent findings regarding the amyloid formation of p53 in vitro and in vivo. We elaborate on prion-like properties of p53 amyloids and their possible involvement in cancer progression. Since the p53 pathway is historically among the most targeted pathway for the development of anti-cancer therapeutics, we have also summarized some of the recent approaches and advances in reviving the anti-proliferative activities of wild-type p53. In this perspective, we provide an insight into understanding p53 as a prion-like protein and propose cancer to be recognized as amyloid or prion-like disease.
This article was published in the following journal.
Most common neurodegenerative diseases feature deposition of protein amyloids and degeneration of brain networks. Amyloids are ordered protein assemblies that can act as templates for their own replic...
Prion diseases are a phenotypically diverse set of disorders characterized by protease-resistant abnormally shaped proteins known as prions. There are three main groups of prion diseases, termed spora...
Prions are unusual protein assemblies that propagate their conformationally-encoded information in absence of nucleic acids. The first prion identified, the scrapie isoform (PrPSc) of the cellular pri...
Prions use cellular machineries for autocatalytic propagation by conformational conversion of the cellular prion protein into the pathological isoform PrP. Autophagy is a basic cellular degradation an...
Prion diseases are devastating neurodegenerative disorders for which no drugs are available. The successful development of therapeutics depends on drug screening platforms and preclinical models that ...
PRION-1 aims to assess the activity and safety of Quinacrine (Mepacrine hydrochloride) in human prion disease. It also aims to establish an appropriate framework for the clinical assessmen...
The purpose of this study to investigate if cases of Creutzfeldt-Jakob Disease (CJD) and other forms of prion disease are being missed in older adults living within Lothian.
The study hypothesis is that that the deleterious effect of prions on the brain may be mediated (at least partially) by activation of serine proteases involved in the coagulation system. I...
This study is designed to better understand the molecular biology of paroxysmal nocturnal hemoglobinuria (PNH) and to determine if prion protein (PrP) functions in long term hematopoietic ...
Postoperative cognitive dysfunction (POCD) can be a serious complication. The development of therapeutic strategies for the prevention and treatment of this condition requires the identifi...
Abnormal isoform of prion proteins (PRIONS) resulting from a posttranslational modification of the cellular prion protein (PRPC PROTEINS). PrPSc are disease-specific proteins seen in certain human and animal neurodegenerative diseases (PRION DISEASES).
A transmissible spongiform encephalopathy (prion disease) of DEER and elk characterized by chronic weight loss leading to death. It is thought to spread by direct contact between animals or through environmental contamination with the prion protein (PRIONS).
Membrane glycosylphosphatidylinositol-anchored glycoproteins that may aggregate into rod-like structures. The prion protein (PRNP) gene is characterized by five TANDEM REPEAT SEQUENCES that encode a highly unstable protein region of five octapeptide repeats. Mutations in the repeat region and elsewhere in this gene are associated with CREUTZFELDT-JAKOB DISEASE; FATAL FAMILIAL INSOMNIA; GERSTMANN-STRAUSSLER DISEASE; Huntington disease-like 1, and KURU.
A cancer registry mandated under the National Cancer Act of 1971 to operate and maintain a population-based cancer reporting system, reporting periodically estimates of cancer incidence and mortality in the United States. The Surveillance, Epidemiology, and End Results (SEER) Program is a continuing project of the National Cancer Institute of the National Institutes of Health. Among its goals, in addition to assembling and reporting cancer statistics, are the monitoring of annual cancer incident trends and the promoting of studies designed to identify factors amenable to cancer control interventions. (From National Cancer Institute, NIH Publication No. 91-3074, October 1990)
A group of genetic, infectious, or sporadic degenerative human and animal nervous system disorders associated with abnormal PRIONS. These diseases are characterized by conversion of the normal prion protein to an abnormal configuration via a post-translational process. In humans, these conditions generally feature DEMENTIA; ATAXIA; and a fatal outcome. Pathologic features include a spongiform encephalopathy without evidence of inflammation. The older literature occasionally refers to these as unconventional SLOW VIRUS DISEASES. (From Proc Natl Acad Sci USA 1998 Nov 10;95(23):13363-83)
Bladder Cancer Brain Cancer Breast Cancer Cancer Cervical Cancer Colorectal Head & Neck Cancers Hodgkin Lymphoma Leukemia Lung Cancer Melanoma Myeloma Ovarian Cancer Pancreatic Cancer ...
The process of gene expression is used by eukaryotes, prokaryotes, and viruses to generate the macromolecular machinery for life. Steps in the gene expression process may be modulated, including the transcription, RNA splicing, translation, and post-tran...