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Rab11-FIP4 interacts with Rab11 in a GTP-dependent manner and its overexpression condenses the Rab11 positive compartment in HeLa cells
Abstract
We have recently identified Rab11-FIP4 as the sixth member of the Rab11-FIP family of Rab11 interacting proteins. Here, we demonstrate that Rab11-FIP4 interacts with Rab11 in a GTP-dependent manner and that its C-terminal region allows the protein to self-interact and interact with pp75/Rip11, Rab11-FIP2, and Rab11-FIP3. However, Rab11-FIP4 does not appear to interact directly with Rab coupling protein (RCP). We investigated the subcellular localisation of Rab11-FIP4 in HeLa cells and show that it colocalises extensively with transferrin and with Rab11. Furthermore, when overexpressed, it causes a condensation of the Rab11 compartment in the perinuclear region. We demonstrate that the carboxy-terminal region of Rab11-FIP4 (Rab11-FIP4(C-ter)) is necessary and sufficient for its endosomal membrane association. Expression of Rab11-FIP4(C-ter) causes a dispersal of the Rab11 compartment towards the cell periphery and does not inhibit transferrin recycling in HeLa cells. It is likely that Rab11-FIP4 serves as a Rab11 effector in a Rab11 mediated function other than transferrin recycling.
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“We found that SH3TC2 interacts with the constitutive active GTP-bound Rab11_Q70L mutants, while there is no binding to the dominant negative guanosine diphosphate-bound Rab11_S25N mutants or to Rab11a_Q70L_I44E, a constitutively active mutant which has a second mutation in its effector domain abrogating effector binding (Wallace et al., 2002) (Fig. 5A and Supplementary Fig. 4B).”
From SH3TC2, a protein mutant in Charcot–Marie–Tooth neuropathy, links peripheral nerve myelination to endosomal recycling (2010) · cites this paper as Wallace et al., 2002
In the citing paper
“while there is no binding to the dominant negative guanosine diphosphate-bound Rab11_S25N mutants or to Rab11a_Q70L_I44E, a constitutively active mutant which has a second mutation in its effector domain abrogating effector binding (Wallace et al., 2002) (Fig. 5A and Supplementary Fig. 4B).”
From SH3TC2, a protein mutant in Charcot–Marie–Tooth neuropathy, links peripheral nerve myelination to endosomal recycling (2010) · cites this paper as Wallace et al., 2002
In the citing paper
“There is at least one known Rab11 effector, Rab11-FIP4, which causes a dramatic condensation of the recycling endosome (Wallace et al., 2002).”
From SH3TC2, a protein mutant in Charcot–Marie–Tooth neuropathy, links peripheral nerve myelination to endosomal recycling (2010) · cites this paper as Wallace et al., 2002
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Cited by
Sorted by citations
Stendel, C., Roos, A., Kleine, H., Arnaud, E., Özçelik, M., Sidiropoulos, P. N. M., Zenker, J., Schüpfer, F., Lehmann, U., Sobota, R. M., et al. (2010) · Brain · doi:10.1093/brain/awq168 · Cited by 102
Metadata
- Authors
- Wallace, D. M. E., Lindsay, A. J., Hendrick, A. G., & McCaffrey, M. W.
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2002-12
- Volume
- 299
- Issue
- 5
- Pages
- 770-779
- ISSN
- 0006-291X
- Cited by
- 57
- References
- 0
- Language
- en
- Funders
- Health Research Board
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