Pauline Isakson

TL;DR: It is demonstrated that expression of several autophagy genes is reduced in Drosophila neural tissues as a normal part of aging, indicating that genetic or age-dependent suppression ofAutophagy is closely associated with the buildup of cellular damage in neurons and a reduced lifespan, while maintaining the expression of a rate-limiting Autophagy gene prevents the age- dependent accumulation of damage in neuron and promotes longevity.

TL;DR: Alfy, a phosphatidylinositol 3-phosphate-binding protein, is central to the selective elimination of aggregated proteins and proposed that Alfy plays a key role in selective macroautophagy by bridging cargo to the molecular machinery that builds autophagosomes.

TL;DR: It is shown here that p62 is required to recruit the large phosphoinositide-binding protein ALFY to cytoplasmic p62 bodies generated upon amino acid starvation or puromycin-treatment, demonstrating that ALFY is required for autophagic degradation of p62-associated ubiquitinated proteins in vivo.

TL;DR: It is found that both all-trans retinoic acid and arsenic trioxide induce autophagy via the mammalian target of rapamycin pathway in APL cells and that autophagic degradation contributes significantly both to the basal turnover as well as the therapy-induced proteolysis of PML/RARA.

TL;DR: The findings indicate that measuring IUP profiles together with an assessment of p62/Ref(2)P proteins can be used as a screening or diagnostic tool to characterize genetic and age-dependent factors that alter the long-term function of autophagy and the clearance of protein aggregates occurring within complex tissues and cells.