ArticleCell death & disease2019
Artificial tethering of LC3 or p62 to organelles is not sufficient to trigger autophagy.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Critical assessment of LC3/GABARAP ligands used for degrader development and ligandability of LC3/GABARAP binding pockets.Nature communications · 2024Article
- Manipulating autophagic degradation in human diseases: from mechanisms to interventions.Life medicine · 2022Review
- Changes of serum P62 and Beclin 1 in patients with pulmonary embolism during treatment and their predictive value for efficacy.American journal of translational research · 2022Article
- Schisandrin B Induced ROS-Mediated Autophagy and Th1/Th2 ImbalanceFrontiers in immunology · 2022Article
- Everolimus and plicamycin specifically target chemoresistant colorectal cancer cells of the CMS4 subtype.Cell death & disease · 2021Article
- Oleate-induced aggregation of LC3 at the trans-Golgi network is linked to a protein trafficking blockade.Cell death and differentiation · 2021Article
- lncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway and Oncogenic Autophagy.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- p62 Overexpression Promotes Bone Metastasis of Lung Adenocarcinoma out of LC3-Dependent Autophagy.Frontiers in oncology · 2021Article
- Rab7-harboring vesicles are carriers of the transferrin receptor through the biosynthetic secretory pathway.Science advances · 2021Article
- Study on Clinical Significance of LncRNA EGOT Expression in Colon Cancer and Its Effect on Autophagy of Colon Cancer Cells.Cancer management and research · 2020Article
- Valproic Acid Enhanced Apoptosis by Promoting Autophagy Via Akt/mTOR Signaling in Glioma.Cell transplantationArticle
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retention using selective hooks (RUSH) system allows to retain a target protein fused to green fluorescent protein (GFP) and a streptavidin-binding peptide (SBP) due to the interaction with a molar excess of streptavidin molecules ("hooks") targeted to selected subcellular compartments. Supplementation of biotin competitively disrupts the interaction between the SBP moiety and streptavidin, liberating the chimeric target protein from its hooks, while addition of avidin causes the removal of biotin from the system and reestablishes the interaction. Based on this principle, we engineered two chimeric proteins involved in autophagy, namely microtubule-associated proteins 1A/1B light chain 3B (MAP1LC3B, best known as LC3) and sequestosome-1 (SQSTM1, best known as p62) to move them as SBP-GFP-LC3 and p62-SBP-GFP at will between the cytosol and two different organelles, the endoplasmic reticulum (ER) and the Golgi apparatus. Although both proteins were functional in thus far that SBP-GFP-LC3 and p62-SBP-GFP could recruit their endogenous binding partners, p62 and LC3, respectively, their enforced relocation to the ER or Golgi failed to induce organelle-specific autophagy. Hence, artificial tethering of LC3 or p62 to the surface of the ER and the Golgi is not sufficient to trigger autophagy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.