Cellular Death & Stress Response
The discovery of autophagy-related ('ATG') proteins in the 1990s greatly advanced the mechanistic understanding of autophagy and clarified the fact that autophagy serves important roles in various biological processes.
Apoptotic caspases belong to the protease enzyme family and are known to play an essential role in inflammation and programmed cell death. Here is the latest research.
An autophagosome is the formation of double-membrane vesicles that involve numerous proteins and cytoplasmic components. These double-membrane vesicles are then terminated at the lysosome where they are degraded. Discover the latest research on autophagosomes here.
The feed focuses on the role of nuclear export inhibitors and their effect on autophagy and the aging process.
Autophagy is an important cellular process for normal physiology and both elevated and decreased levels of autophagy are associated with disease. Here is the latest research.
Autophagy preserves the health of cells and tissues by replacing outdated and damaged cellular components with fresh ones. In starvation, it provides an internal source of nutrients for energy generation and, thus, survival. A powerful promoter of metabolic homeostasis at both the cellular and whole-animal level, autophagy prevents degenerative diseases. It does have a downside, however--cancer cells exploit it to survive in nutrient-poor tumors.
Autophagy is a cellular process that allows degradation by the lysosome of cytoplasmic components such as proteins or organelles. Here is the latest research on autophagy & model organisms
Autophagy is a lysosomal pathway that involves degradation of proteins and functions in normal growth and pathological conditions, through a series of complex networks. The catabolic process involves delivery of proteins and organelles to the lysosome. Here is the latest research on autophagy networks.
Autophagy leads to degradation of damaged proteins and organelles by the lysosome. Impaired autophagy has been implicated in several diseases. Here is the role of autophagy in cancer and Parkinson’s.
BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.
Caspases, the family of cysteine proteases are involved in programmed cell death, but their role in metabolic diseases, inflammation and immunity has been of interested. Discover the latest research on caspases in metabolic diseases here.
This feed focuses on cellular aging with emphasis on the mitochondria, autophagy, and metabolic processes associated with aging and longevity. Here is the latest research on cell aging.
Development of gene editing techniques, including CRISPR and TALENs, has relied on mechanisms that underlie DNA repair and genome stability pathways. This feed focuses on the role of DNA repair mechanisms in gene editing and genetic engineering.
Cells are subjected to several DNA damaging events on a daily basis which results in the induction of DNA damage signaling and repair cascades to ensure genomic integrity. Here is the latest research on DNA damage signaling and repair mechanisms in primary cells.
Death receptors are members of the tumour necrosis alpha superfamily that contain a death domain. They mediate a variety of different cellular functions including apoptosis.
This membrane trafficking pathway is important in the degradation of proteins and organelles and involves the formation of double membrane autophagosomes that are transported to the lysosome. Here is the latest research on membrane trafficking in autophagy.
Autophagy is thus a key determinant for mitochondrial health and proper cell function. In addition to autophagy's significance in mitochondrial integrity, several lines of evidence suggest that mitochondria can also substantially influence the autophagic process.
Given that progression of neurodegenerative diseases can be driven by aggregation of misfolded proteins, autophagic activity is through to modulate the severity of neurodegenerative diseases. Here is the latest research on the influence of autophagy on neurodegeneration.
Poly(ADP-Ribose) Polymerase (PARP) is an enzyme with several functions, including cell differentiation, proliferation, and DNA damage repair. Here is the latest research on PARP.
The redox theory of aging is that aging is a decline in plasticity of genome-exposome interaction that occurs as a consequence of execution of differentiation and exposure memory systems. This includes compromised mitochondrial and bioenergetic flexibility, impaired food utilization and metabolic homeostasis, decreased barrier and defense capabilities and loss of reproductive fidelity and fecundity. This theory accounts for hallmarks of aging, including failure to maintain oxidative or xenobiotic defenses, mitochondrial integrity, proteostasis, barrier structures, DNA repair, telomeres, immune function, metabolic regulation and regenerative capacity.
This feed focuses on the role of the proteosome and lysosome in degrading mitochondria of Retinal Ganglion Cells (RGC). Mitochondrial dysfunction in RGCs may lead to optical neuropathies.
Selective autophagy has been found to be a critical mediator for cellular homeostasis involved with the turnover of proteins, protein aggregates, organelles and pathogens. It has been characterized by distinct cargo receptors that undergo specific mechanisms for degradation. Here is the latest research on selective autophagy.
Senotherapeutics, which selectively kill senescent cells (senolytics) or to suppress the senescence-associated secretory phenotype (SASP) that drives sterile inflammation associated with ageing (senomorphics), have been implicated to be novel strategy for aging intervention applicable to promote healthy aging and to prevent or treat age-related diseases
Autophagy is an important process in degradation of proteins and organelles, survival during nutrient starvation and cellular remodelling. It is regulated by a complex network of signaling cascades. Discover the latest research on signal regulation of autophagy initiation here.