This volume provides a comprehensive collection of experimental protocols for investigating ferroptosis in different systems, including cultured cells, animal models, and human tissues. The techniques covered in this book look at various aspects of ferroptosis ranging from the detection of lipid peroxidation to the measurement of glutathione peroxidase activity and the evaluation of mitochondrial morphology. Chapters also discuss basic molecular biology methods such as quantitative PCR and immunoblotting, and advanced imaging techniques such as transmission electron microscopy and confocal fluorescence microscopy. Written in the highly successful Methods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and tips on troubleshooting and avoiding known pitfalls. Cutting-edge and authoritative, Ferroptosis: Methods and Protocols is a valuable resource for researchers who are interested in studying ferroptosis in different contexts including basic research, drug discovery, and clinical applications.

Molecular Characterization of Autophagic Responses, Part B presents a collection of methods for the qualitative and quantitative evaluation of virtually all the morphological, biochemical, and functional manifestations of autophagy, in vitro, ex vivo and in vivo, in organisms as distant as yeast and man. Autophagy is an evolutionarily conserved mechanism for the lysosomal degradation of superfluous or dangerous cytoplasmic entities, and plays a critical role in the preservation of cellular and organismal homeostasis. Monitoring the biochemical processes that accompany autophagy is fundamental for understanding whether autophagic responses are efficient or dysfunctional.

Cell senescence is the process whereby cells permanently lose the possibility to proliferate without undergoing cell death, and occurs in a plethora of distinct model organisms. In Cell Senescence: Methods and Protocols, expert researchers in the field detail the methods that are now commonly used to study cell senescence, in model organisms encompassing bacteria, fungi, worms, flies, zebrafish, and mammalian cells. These techniques cover the study of all the morphological, biochemical and functional manifestations of senescence at the cellular level and include protocols for population analyses and high-throughput approaches in suitable model organisms. Written in the highly successful Methods in Molecular Biology (TM) series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and key tips on troubleshooting and avoiding known pitfalls.

Cell senescence is the process whereby cells permanently lose the possibility to proliferate without undergoing cell death, and occurs in a plethora of distinct model organisms. In Cell Senescence: Methods and Protocols, expert researchers in the field detail the methods that are now commonly used to study cell senescence, in model organisms encompassing bacteria, fungi, worms, flies, zebrafish, and mammalian cells. These techniques cover the study of all the morphological, biochemical and functional manifestations of senescence at the cellular level and include protocols for population analyses and high-throughput approaches in suitable model organisms. Written in the highly successful Methods in Molecular Biology (TM) series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and key tips on troubleshooting and avoiding known pitfalls.

This new volume of Methods in Enzymology continues the legacy of this premier serial with quality chapters authored by leaders in the field. This volume covers research methods providing a a theoretical overview on metabolic alterations of cancer cells and a series of protocols that can be employed to study oncometabolism, in vitro, ex vivo and in vivo. Malignant cells exhibit metabolic changes when compared to their normal counterparts, owing to both genetic and epigenetic alterations. Although such a metabolic rewiring has recently been indicated as "yet another" general hallmark of cancer, accumulating evidence suggests that the metabolic alterations of each neoplasm rather represent a molecular signature that intimately accompanies, and hence cannot be severed from, all facets of malignant transformation.
Continues the legacy of this premier serial with quality chapters authored by leaders in the fieldCovers research methods in biomineralization scienceContains sections on such topics providing a a theoretical overview on metabolic alterations of cancer cells and a series of protocols that can be employed to study oncometabolism, in vitro, ex vivo and in vivo."

Volume 542 of "Methods in Enzymology" continues the legacy of this premier serial with quality chapters authored by leaders in the field. This new volume covers research methods providing a theoretical overview on metabolic alterations of cancer cells and a series of protocols that can be employed to study oncometabolism, in vitro, ex vivo and in vivo. Malignant cells exhibit metabolic changes when compared to their normal counterparts, owing to both genetic and epigenetic alterations. Although such a metabolic rewiring has recently been indicated as "yet another" general hallmark of cancer, accumulating evidence suggests that the metabolic alterations of each neoplasm rather represent a molecular signature that intimately accompanies, and hence cannot be severed from, all facets of malignant transformation.
Continues the legacy of this premier serial with quality chapters authored by leaders in the field Covers research methods in biomineralization scienceProvides theoretical overview on metabolic alterations of cancer cells, and a series of protocols that can be employed to study oncometabolism, in vitro, ex vivo and in vivo

Molecular Characterization of Autophagic Responses, Part A, presents a collection of methods for the qualitative and quantitative evaluation of virtually all the morphological, biochemical, and functional manifestations of autophagy, in vitro, ex vivo and in vivo, in organisms as distant as yeast and man. Autophagy is an evolutionarily conserved mechanism for the lysosomal degradation of superfluous or dangerous cytoplasmic entities, and plays a critical role in the preservation of cellular and organismal homeostasis. Monitoring the biochemical processes that accompany autophagy is fundamental for understanding whether autophagic responses are efficient or dysfunctional.

In any movement of their life, immune cells, especially T and B lymphocytes, are confronted with an essential choice: to continue their existence or to commit a sort of metabolic suicide that is referred to as apoptosis or programmed cell death. In contrast to most philosophers, lymphocytes and their precursors are constantly susceptible to suicide, and it even appears that the usual cause of T or B cell elimination is suicide rather than death from natural causes, accidents or murder. This book provides a vast overview of lymphocytes suicide: external triggers and internal motives leading to suicidal impulses, accomplices in self-destruction, weapons implicated in self-execution, removal of dead bodies and pharmacological prevention of suicide. Most of the chapters in this book are devoted to the physiology of apoptosis. The goal is to unmask the external triggers of apoptosis, unravel the signal transduction pro cesses involved therein and describe the role of oncogenes, "death genes" and effector molecules in the apoptotic cas cade. The remaining chapters deal with the pathophysiologi cal aspects of lymphocyte apoptosis, namely, as a host contribution to HIV-induced lymphopenia, and therapeutic strategies for the avoidance of lymphocyte death. We are confident that this compendium will contribute to the exploration of cellular suicide, not only from a basic scientist's viewpoint but also with regard to the possible clinical implications of apoptosis (dys)regulation. Far from having a depressing effect on the reader, cellular suicide may thus provide a source of both intellectual excitement and therapeutic inspiration."

In 1920s, Otto Warburg described the phenomenon of aerobic glycolysis, the ability of tumour cells to convert glucose to lactate in the presence of normal oxygen conditions. Warburg 's hypothesis of an altered metabolism in cancer cells found no immediate acceptance, though it was latter confirmed for most human tumours. With the advent of molecular biology the focus in tumour research has shifted towards the search for oncogenes. However, the interest in cancer molecular profiling eventually led to a renaissance of the Warburg effect trying to combine genetic alterations with effects on metabolism with the help of modern analytic technologies to rapidly analyze broad varieties of metabolites in various tissues and bodyfluids (metabonomics).