ArticleSmall GTPases2016
A fresh look at the function of Rabaptin5 on endosomes.
Article in Small GTPases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Survey of nucleotide-specific Rab GTPase interactions reveals multiple Rab effectors.bioRxiv : the preprint server for biology · 2026Article
- ESCRTing the RABs through conversion.Biochemical Society transactions · 2025Review
- Host factor Rab4b mediates internalization and intoxication of 3D4/21 cells by the active subunit of theFrontiers in microbiology · 2025Article
- Protein sorting from endosomes to the TGN.Frontiers in cell and developmental biology · 2023Review
- Retrograde transport of CDMPR depends on several machineries as analyzed by sulfatable nanobodies.Life science alliance · 2022Article
- Rabaptin5 targets autophagy to damaged endosomes and Salmonella vacuoles via FIP200 and ATG16L1.EMBO reports · 2022Article
- Phosphorylated Heat Shock Protein 27 Inhibits Lipopolysaccharide-Induced Inflammation in Thp1 Cells by Promoting TLR4 Endocytosis, Ubiquitination, and Degradation.Inflammation · 2019Article
- The Known and Potential Intersections of Rab-GTPases in Human Papillomavirus Infections.Frontiers in cell and developmental biology · 2019Review
- Kinesin-2 Controls the Motility of RAB5 Endosomes and Their Association with the Spindle in Mitosis.International journal of molecular sciences · 2018Article
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
No grant is acknowledged in the PubMed record.
Abstract
Rab GTPases act as organizers of protein networks defining identities and functions of organelles of the endocytic and secretory pathways. Various modes of coordination between different Rabs drive the timely maturation and conversion of membranes. Endosomal Rab5 has been known as the prime example for self-activation via a feedback loop recruiting Rabaptin5, which is complexed with the Rab5 exchange factor Rabex5, and couples to Rab4-GTP. Among other effectors, Rab5 also recruits the Mon1/SAND1-Ccz1 complex that both activates Rab7 and dissociates Rabex5 for Rab5-to-Rab7 conversion of early-to-late endosomes. A detailed deletion analysis now revealed 2 separate binding sites each for Rab4-GTP and Rab5-GTP and indicates a feedforward mechanism of Rab5 activation. Rabaptin5/Rabex5 is recruited to endosomal membranes positive for Rab4-GTP and ubiquitinated cargo (binding to the ubiquitin binding site of Rabex5). This mechanism also suggests additional criteria for Rab5 inactivation concomitant with increasing Rab7-GTP levels. The disappearance of ubiquitinated cargo upon ESCRT-mediated formation of intraluminal vesicles and inactivation of Rab4 may also contribute to loss of Rab5 activation. Rabaptin5/Rabex5 thus may integrate several cues of maturation to perform Rab conversion. Furthermore Rab5 binding to Rabaptin5 appears to prevent uncontrolled progression to late endosomes.
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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.