RanBP1 is crucial for the release of RanGTP from importin β-related nuclear transport factors

Nucleocytoplasmic transport appears mediated by shuttling transport receptors that bind RanGTP as a means to regulate interactions with their cargoes. The receptor·RanGTP complexes are kinetically very stable with nucleotide exchange and GTP hydrolysis being blocked, predicting that a specific disas...

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Veröffentlicht in:FEBS letters 1997-12, Vol.419 (2), p.249-254
Hauptverfasser: Bischoff, F.Ralf, Görlich, Dirk
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description Nucleocytoplasmic transport appears mediated by shuttling transport receptors that bind RanGTP as a means to regulate interactions with their cargoes. The receptor·RanGTP complexes are kinetically very stable with nucleotide exchange and GTP hydrolysis being blocked, predicting that a specific disassembly mechanism exists. Here we show in three cases receptor·RanGTP·RanBP1 complexes to be the key disassembly intermediates, where RanBP1 stimulates the off-rate at the receptor/RanGTP interface by more than two orders of magnitude. The transiently released RanGTP·RanBP1 complex is then induced by RanGAP to hydrolyse GTP, preventing the receptor to rebind RanGTP. The efficient release of importin β from RanGTP requires importin α, in addition to RanBP1.
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subjects Animals
beta Karyopherins
Biological Transport
CAS
Cell Nucleus - metabolism
GAP
GDP-bound form of Ran
GTP-Binding Proteins - metabolism
GTP-bound form of Ran
GTPase activating protein
Guanosine Triphosphate - metabolism
Humans
Importin
Mice
NPC
nuclear pore complex
Nuclear Proteins - metabolism
Nuclear transport
ran GTP-Binding Protein
RanBP1
RanGDP
RanGTP
Receptors, Cytoplasmic and Nuclear - metabolism
Recombinant Proteins - metabolism
Transportin
title RanBP1 is crucial for the release of RanGTP from importin β-related nuclear transport factors
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