Pa28y Affects Cellular Resolution Of Oxidative Dna Damage

Summary: Increased levels of reactive oxygen species (ROS) are present in almost all cancers. Since increased levels of ROS can cause serious damage to nucleic acids, carbohydrates, lipids and proteins, understanding how cancer cells sustain their altered biology could identify ways to selectively target transformed cells. ... Here, we identify an expanded role for PA28y in the cellular response to oxidative stress. ... Taken together, our data reveal an expanded role for PA28y in the cellular response to oxidative damage, perhaps playing an important role in the recognition of oxidatively-damaged DNA. -- Abstract.

This book, written by members of the European network PROTEOSTASIS, provides an up-to-date review of the research regarding protein homeostasis in health and disease. With new discoveries contributing to the increasing complexity of this topic, the book offers a detailed overview of the pathways regulating protein homeostasis, including autophagy and the ubiquitin protein family. Following a basic introduction, it explains how defects in protein homeostasis contribute to numerous pathologies, including cancer, neurodegeneration, inflammation and a number of rare diseases. In addition, it discusses, the role of protein homeostasis in cellular development and physiology. Highlighting the latest research in the field of protein homeostasis and its implications for various clinically relevant diseases, the book appeals to researchers and clinicians, while also offering a reference guide for scholars who are new to the field.

Covering all major components of the ocular system, this state-of-the-art text is essential for vision scientists, biomedical engineers, and advanced clinicians with an interest in the role of mechanics in ocular function, disease, therapeutics, and surgery. With every chapter, leading experts strengthen the arguments that biomechanics is an indispensable and rapidly evolving tool for understanding and managing ocular disease.

Protein degradation has been identified as a major mechanism for the regulation of cellular functions. Not surprisingly, its deregulation is implied in almost any pathological condition. This book describes how aged proteins are eliminated during cell metabolism, how cell proliferation is regulated by protein degradation and how its deregulation can contribute to the development of cancer, how protein degradation is modified during normal and abnormal aging, in particular with regard to Alzheimer's disease and other degenerative diseases of the brain and central nervous system. Attempts aiming at correcting these pathologies by interfering with deviations of the normal pathway of protein degradation are also treated.