Autophagy is a normal process in which a cell destroys proteins and other substances in its cytoplasm (the fluid inside the cell membrane but outside the nucleus), which may lead to cell death. Autophagy may prevent normal cells from developing into cancer cells, but it may also protect cancer cells by destroying anticancer drugs or substances taken up by them.
The SARS-CoV-2 virus may enter and replicate in human cells by exploiting newly-identified sequences within cell receptors, according to work from two teams of scientists.
Autophagy is a fundamental cellular process by which cells capture and degrade their own dysfunctional or superfluous components for degradation and recycling.
Kanazawa University’s pioneering high-speed atomic force microscope technology has now shed light on the structure and dynamics of some of life’s most ubiquitous and inscrutable molecules – intrinsically disordered proteins.
The research group led by Dr Sjoerd van Wijk from the Institute of Experimental Cancer Research in Paediatrics at Goethe University already two years ago found evidence indicating that the anti-diarrhea drug loperamide could be used to induce cell death in glioblastoma cell lines.
A drug that boosts the removal of cellular debris in immune cells may increase the protective effects of vaccines in older adults, a study published today in eLife shows.
Drs. Nobuo Noda (Director) and Kazuaki Matoba (Senior Researcher) et al. at the Institute of Microbial Chemistry (BIKAKEN, Tokyo, Japan) discovered that Atg9, one of the proteins that function to mediate autophagy, has phospholipid-translocation activity (the lipid scramblase activity) between the two layers of the lipid bilayer and elucidated that the protein's activity brings about autophagosome membrane expansion.
Liver cancer from too much fat accumulation in the liver has been increasing in many countries including Japan. In order to change this unfortunate state of affairs, it is important to improve the prognosis of non-alcoholic fatty liver disease.
SPIN (SPermidin and eugenol INtegrator for the contrasting incidence of coronavirus in EU population) is a European project powered by EIT Food that is currently developing a dietary supplement supporting the function of the immune system in the fight against SARS-CoV-2 infections in the population at high risk.
In a healthy brain, the multistep waste clearance process known as autophagy routinely removes and degrades damaged cell components - including malformed proteins like tau and toxic mitochondria.
Human cells are required to work similar to well-oiled machines to maintain the proper function of individuals’ body.
A team of researchers have plotted the genes that enable cancer cells to avoid being destroyed by the immune system.
Scientists have created an animal model that simulates cerebellar neurodegeneration and motor dysfunction.
A congenital disorder of the fat metabolism can apparently cause chronic hyperreaction of the immune system. This is the conclusion reached by researchers from the University of Bonn in a recent study.
People may go to great lengths to fight aging, but this process is a part of life.
Non-alcoholic fatty liver disease is the most common chronic liver disease in the world, with sometimes life-threatening consequences.
Huntington disease is a progressive debilitating brain disorder that causes uncontrolled movements, psychological problems, and loss of cognition.
Chaperone-mediated autophagy (CMA) is a self-eating process that occurs in embryonic stem cells.
A team of researchers have analyzed the degradation mechanism of the endoplasmic reticulum (ER) called ER-phagy.
The idea of the cell as a city is a common introduction to biology, conjuring depictions of the cell's organelles as power plants, factories, roads, libraries, warehouses and more.
Researchers at TMIMS have revealed that PINK1 (a serine/threonine kinase) and Parkin (a ubiquitin ligating enzyme: E3) work together to ubiquitylate the outer membrane proteins of damaged mitochondria to induce selective autophagy called mitophagy.