Formation and release of arrestin domain-containing protein 1-mediated microvesicles (ARMMs) at plasma membrane by recruitment of TSG101 protein
By J. Nabhan, Ruoxi Hu, R. Oh, Stanley N Cohen, Q. Lu. Proceedings of the National Academy of Sciences of the United States of America, 2012
632 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/461b377751cd289aee6585380595cda9cb48ef68
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- C. Théry
- G. Raposo
- Marina Colombo
- X. Breakefield
- Suresh Mathivanan
- Hina Kalra
- W. Stoorvogel
- G. Drummen
In Physiology
Citations in the corpus
- Exosomes and microvesicles: extracellular vesicles for genetic information transfer and gene therapy. (2012, background): “However, increasing evidence now indicates Exosome Homogenous population with a size of 40–100 nm in diameter End of endocytic pathway, released from cells when multivesicular bodies fuse with the plasma membrane (16,103,117) Exosomal markers include CD9, CD63, Alix, flotillin-1 and Tsg101 ESCRT is ”
- Introduction to Extracellular Vesicles: Biogenesis, RNA Cargo Selection, Content, Release, and Uptake (2016, neutral): “…recruitment of the ESCRT-I subunit TSG101 to the plasma membrane through its binding to a tetrapeptide protein within the Arrestin 1 domain–containing protein 1 (ARRDC1), resulting in the release of MVs containing TSG101, ARRDC1, and other cellular proteins (Nabhan et al. 2012; Tauro et al. 2012).”
- Exosome Theranostics: Biology and Translational Medicine (2018, background): “Some vesicles that have a diameter of >150 nm can be generated by an endosomal pathway [29], and other vesicles of <150 nm in diameter can bleb directly from the plasma membrane [30, 31].”
- Biomolecular Fluorescence Complementation Profiling and Artificial Intelligence Structure Prediction of the Kaposi’s Sarcoma-Associated Herpesvirus ORF18 and ORF30 Interaction (2022, neutral): “mCherry-TSG101 [27] (Addgene plasmid # 38318; gifted from Dr.”
- Focus on Extracellular Vesicles: Introducing the Next Small Big Thing (2016, background): “Nabhan and co-workers showed that budding at the PM is driven by the interaction of the TSG101 subunit of ESCRT-I with the tetrapeptide PSAP motif of arrestin domain-containing protein 1 (ARRDC1); the N-terminal arrestin domain of ARRDC1 directs PM targeting [55].”
- SORTING IT OUT: REGULATION OF EXOSOME LOADING (2014, background): “These vesicles are CD63-negative and their secretion seems to be driven by interaction of the PSAP motif of ARRDC with the UEV motif of tsg101.”
- Advances in therapeutic applications of extracellular vesicles (2019, background): “Using chimeric proteins consisting of a protein of interest fused to ARRDC1, which drives the budding of ARMMs from the plasma membrane (144), the authors demonstrated functional delivery of the tumor suppressor p53 protein (ARRDC1-p53) in vivo.”
- Biogenesis, secretion, and intercellular interactions of exosomes and other extracellular vesicles. (2014, background): “Localization of gag or ARRDC1 at the PM directs EV outward budding there, instead of into MVBs.”
- Extracellular vesicles: Exosomes, microvesicles, and friends (2013, background): “Interestingly, a recent study provided evidence for the recruitment of the ESCRT-I subunit Tsg101 to the plasma membrane by means of a tetrapeptide PSAP motif that drives the ARRDC1 (Arrestin 1 domain–containing protein 1) into MVs (Nabhan et al., 2012).”
- Syndecan–syntenin–ALIX regulates the biogenesis of exosomes (2012, background): “Note that truncated forms of Alix containing the V domain interact with the two parts of the N-Ter domain of syntenin that contain LYPXL motifs, (1-30) and (31-60), and that mutation of the three LYPXL motifs (YP to AA) abolishes the interaction.”