Recently, it has emerged that crucial regulators of cell death pathways also play key unconventional roles in several intracellular processes. For example, Bcl-2 family of proteins, composed of a network of pro- and anti-apoptotic members, are well-known to mediate the ‘intrinsic’ apoptosis pathway by controlling mitochondrial outer membrane integrity. However, accumulating evidence reveals that Bcl-2 proteins also control mitochondrial dynamics and functions, such as mitochondrial fusion/fission events, as well as bioenergetics and Ca 2+ homeostasis at the mitochondrial and ER level. Similarly, proteases and kinases, such as Caspases and RIPKs, that are pivotal for inflammation, extrinsic apoptosis and alternative cell death pathways, have been implicated in proteostasis, reorganization of the cytoskeleton, cell division but also in neuronal behavior. These alternative functions of key cell death proteins open a new era in our understanding of how life and death processes in cells are tightly interconnected, and may provide novel insights into mechanisms of development and disease.
The goal of the proposed research topic is to achieve a better understanding of the physiological and pathological roles of cell death proteins beyond their well-known functions. We aim to provide a summary of existing knowledge and incorporate it with novel studies that tackle unexplored cell death pathways, protein network interactions and their mechanisms of action, ultimately seeking new awareness into the development of the disease and possibly discovering unique therapeutic targets. Hence, we encourage researchers to submit studies, including original research articles,
methods, review and mini-review on the involvement of unconventional roles of cell death proteins during development, health and disease.
The scope of this Research Topic is to highlight both new developments and the current challenges of studying the unconventional roles of cell death proteins. Reports submitted can cover, but are not limited to:
- Novel roles of cell death proteins in development, health and disease, including studies on several types of cellular, animal and clinical models of cancer and/or neurological disorders;
- Identification of unique physiological ‘daytime’ functions of cell death proteins/signaling;
- Involvement of cell death proteins in Ca 2+ homeostasis, mitochondrial function, bioenergetics and cellular metabolism;
- Original roles of the cell death proteins, including Bcl-2 family members, caspases, proteases, receptors, neurodevelopmental proteins and so on;
- Pathophysiological outcome caused by dysregulation of unconventional functions of cell death proteins/signaling;
- Mechanisms and mathematical/computational modelling of non-apoptotic functions of cell death proteins/signaling;
- Innovative roles of these proteins in alternative cell death pathways;
- Discovery or development of new therapeutics aimed to target these non-apoptotic functions of cell death proteins/signaling;
- Methodological techniques to investigate cell death signaling.
Recently, it has emerged that crucial regulators of cell death pathways also play key unconventional roles in several intracellular processes. For example, Bcl-2 family of proteins, composed of a network of pro- and anti-apoptotic members, are well-known to mediate the ‘intrinsic’ apoptosis pathway by controlling mitochondrial outer membrane integrity. However, accumulating evidence reveals that Bcl-2 proteins also control mitochondrial dynamics and functions, such as mitochondrial fusion/fission events, as well as bioenergetics and Ca 2+ homeostasis at the mitochondrial and ER level. Similarly, proteases and kinases, such as Caspases and RIPKs, that are pivotal for inflammation, extrinsic apoptosis and alternative cell death pathways, have been implicated in proteostasis, reorganization of the cytoskeleton, cell division but also in neuronal behavior. These alternative functions of key cell death proteins open a new era in our understanding of how life and death processes in cells are tightly interconnected, and may provide novel insights into mechanisms of development and disease.
The goal of the proposed research topic is to achieve a better understanding of the physiological and pathological roles of cell death proteins beyond their well-known functions. We aim to provide a summary of existing knowledge and incorporate it with novel studies that tackle unexplored cell death pathways, protein network interactions and their mechanisms of action, ultimately seeking new awareness into the development of the disease and possibly discovering unique therapeutic targets. Hence, we encourage researchers to submit studies, including original research articles,
methods, review and mini-review on the involvement of unconventional roles of cell death proteins during development, health and disease.
The scope of this Research Topic is to highlight both new developments and the current challenges of studying the unconventional roles of cell death proteins. Reports submitted can cover, but are not limited to:
- Novel roles of cell death proteins in development, health and disease, including studies on several types of cellular, animal and clinical models of cancer and/or neurological disorders;
- Identification of unique physiological ‘daytime’ functions of cell death proteins/signaling;
- Involvement of cell death proteins in Ca 2+ homeostasis, mitochondrial function, bioenergetics and cellular metabolism;
- Original roles of the cell death proteins, including Bcl-2 family members, caspases, proteases, receptors, neurodevelopmental proteins and so on;
- Pathophysiological outcome caused by dysregulation of unconventional functions of cell death proteins/signaling;
- Mechanisms and mathematical/computational modelling of non-apoptotic functions of cell death proteins/signaling;
- Innovative roles of these proteins in alternative cell death pathways;
- Discovery or development of new therapeutics aimed to target these non-apoptotic functions of cell death proteins/signaling;
- Methodological techniques to investigate cell death signaling.