2021
DOI: 10.18632/aging.203297
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Inhibition of heat shock proteins increases autophagosome formation, and reduces the expression of APP, Tau, SOD1 G93A and TDP-43

Abstract: Aberrant expression and denaturation of Tau, amyloid-beta and TDP-43 can lead to cell death and is a major component of pathologies such as Alzheimer’s Disease (AD). AD neurons exhibit a reduced ability to form autophagosomes and degrade proteins via autophagy. Using genetically manipulated colon cancer cells we determined whether drugs that directly inhibit the chaperone ATPase activity or cause chaperone degradation and endoplasmic reticulum stress signaling leading to macroautophagy could reduce the levels … Show more

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Cited by 12 publications
(19 citation statements)
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“…In HCN2 neuronal cells and BV2 microglial cells, knock down of the essential LAP regulatory protein Rubicon suppressed autophagosome formation though did not appear to alter autophagic ux with respect to the formation of autolysosomes, i.e., vesicles that were initially GFP+ RFP+ became over time only RFP+ (Figure 1). Knock down of Beclin1 or ATG5 abolished autophagosome formation and autophagic ux (Figure 2) [10]. HCN2 neuronal and BV2 microglial cells were transfected with plasmids to express Tau or APP, and co-transfected with siRNA molecules to knock down the expression of Rubicon, Beclin1 or ATG5.…”
Section: Resultsmentioning
confidence: 97%
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“…In HCN2 neuronal cells and BV2 microglial cells, knock down of the essential LAP regulatory protein Rubicon suppressed autophagosome formation though did not appear to alter autophagic ux with respect to the formation of autolysosomes, i.e., vesicles that were initially GFP+ RFP+ became over time only RFP+ (Figure 1). Knock down of Beclin1 or ATG5 abolished autophagosome formation and autophagic ux (Figure 2) [10]. HCN2 neuronal and BV2 microglial cells were transfected with plasmids to express Tau or APP, and co-transfected with siRNA molecules to knock down the expression of Rubicon, Beclin1 or ATG5.…”
Section: Resultsmentioning
confidence: 97%
“…Previously we had shown that AR12 and neratinib reduced Tau and APP levels via macro-autophagy and that cells expressing the autophagy protein ATG16L1 T300 were more capable of autophagosome formation and APP / Tau degradation than cells expressing the ATG16L1 A300 isoform [10]. In the present studies, knock down of a regulator of LC3-associated phagocytosis / endocytosis, Rubicon, signi cantly reduced the abilities of the drugs alone or in combination to reduce the expression of chaperone proteins, Tau and APP.…”
Section: Discussionmentioning
confidence: 98%
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