ArticleDevelopmental cell2010
Rapid inactivation of proteins by rapamycin-induced rerouting to mitochondria.
Article in Developmental cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
153 citing papers in PubMed, 259 citations in OpenAlex.
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- HOPS/CORVET tethering complexes are critical for endocytosis and protein trafficking to invasion related organelles in malaria parasites.PLoS pathogens · 2025Article
- Acute diacylglycerol production activates critical membrane-shaping proteins leading to mitochondrial tubulation and fission.Nature communications · 2025Article
- HPV16 entry requires dynein for minus-end transport and utilizes kinesin Kif11 for plus-end transport along microtubules during mitosis.Journal of virology · 2025Article
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- The role of the AP-1 adaptor complex in outgoing and incoming membrane traffic.The Journal of cell biology · 2024Article
- Kinesin Regulation in the Proximal Axon is Essential for Dendrite-selective Transport.Molecular biology of the cell · 2024Article
- Polarized transport requires AP-1-mediated recruitment of KIF13A and KIF13B at the trans-Golgi.Molecular biology of the cell · 2024Article
93 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We have developed a method for rapidly inactivating proteins with rapamycin-induced heterodimerization. Cells were stably transfected with siRNA-resistant, FKBP-tagged subunits of the adaptor protein (AP) complexes of clathrin-coated vesicles (CCVs), together with an FKBP and rapamycin-binding domain-containing construct with a mitochondrial targeting signal. Knocking down the endogenous subunit with siRNA, and then adding rapamycin, caused the APs to be rerouted to mitochondria within seconds. Rerouting AP-2 to mitochondria effectively abolished clathrin-mediated endocytosis of transferrin. In cells with rerouted AP-1, endocytosed cation-independent mannose 6-phosphate receptor (CIMPR) accumulated in a peripheral compartment, and isolated CCVs had reduced levels of CIMPR, but normal levels of the lysosomal hydrolase DNase II. Both observations support a role for AP-1 in retrograde trafficking. This type of approach, which we call a "knocksideways," should be widely applicable as a means of inactivating proteins with a time scale of seconds or minutes rather than days.
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Registered trials
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.