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Autophagy was first observed by Keith R. Porter and his student Thomas Ashford at the Rockefeller Institute.In January 1962 they reported an increased number of lysosomes in rat liver cells after the addition of glucagon, and that some displaced lysosomes towards the centre of the cell contained other cell organelles such as mitochondria.
Chaperone-mediated autophagy (CMA) ... CMA is active at all times in different tissues (liver, kidney, brain), and almost all cell types in culture studied. However ...
Autophagy database offers comparison of homologous proteins between 41 different species to search new and old autophagy-related proteins, so that current autophagy research can be streamlined. [1] The database was made publicly available in March 2010 and currently includes 7,444 genes/proteins in 82 eukaryotes.
Rubicon (run domain Beclin-1-interacting and cysteine-rich domain-containing protein) is a protein that in humans is encoded by the RUBCN gene. [5] [6] Rubicon is one of the few known negative regulators of autophagy, a cellular process that degrades unnecessary or damaged cellular components. [7]
Autophagy is an important cellular process that helps in maintaining homeostasis. It goes through destroying and recycling the cytoplasmic organelles and macromolecules. During the initiation of autophagy, ATG7 acts like an E-1 enzyme for ubiquitin-like proteins (UBL) such as ATG12 and ATG8. ATG7 helps these UBL proteins in targeting their ...
He was also the first to understand the process of cell eating, which he called "cytolysomes," now known as autophagy, another Nobel Prize-winning discovery. He developed the method for making liver cancer cells, later called Novikoff hepatoma, which paved the way for cellular experiments in cancer studies.
Atg1 is a kinase upregulated upon induction of autophagy. Atg13 regulates Atg1 and together they form a complex called Atg13:Atg1, which receives signals from the master of nutrient sensing – Tor. Atg1 is also important in late stages of autophagosome formation. [8]
Holistically, chaperone-mediated autophagy is disrupted with impaired WASH complex function; heterozygous-VPS35 knockout mice and mice with the VPS35-D620N mutation have a reduction in LAMP2a trafficking, which leads to α-synuclein accumulation in the brain and poses an important functional implication in PD. [8] [10]