Several studies link the formation of beta amyloid plaques in Alzheimer's disease to mammalian target of rapamycin's negativeregulation of this process. Experiments increasing the level of Beclin1 expression in mice, thus positively regulating thisprocess, provide proof of this process's role in tumor suppression. Cvt targeting in yeast uses this process, which is initiated bythe ULK1 kinase complex. Evidence for this process can be confiÂrmed visually by dot-like or ring-like patterns in immunoflfluorescentstains of LC3, a homolog of the critical Atg markers. The "micro" form of this process is direct, whereas the "
Several studies link the formation of beta amyloid plaques in Alzheimer's disease to mammalian target of rapamycin's negativeregulation of this process. Experiments increasing the level of Beclin1 expression in mice, thus positively regulating thisprocess, provide proof of this process's role in tumor suppression. Cvt targeting in yeast uses this process, which is initiated bythe ULK1 kinase complex. Evidence for this process can be confiÂrmed visually by dot-like or ring-like patterns in immunoflfluorescentstains of LC3, a homolog of the critical Atg markers. The "micro" form of this process is direct, whereas the "macro"form, which is canonically induced by stress or starvation, results in the formation of a double-membrane organelle aroundthe target cytoplasmic components. For 10 points, name this process in which lysosomes are fused to degraded cell parts, thusallowing the cell to "eat itself."
Several studies link the formation of beta amyloid plaques in Alzheimer's disease to mammalian target of rapamycin's negativeregulation of this process.
autophagy