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Titlebook: ARF Family GTPases; Richard A. Kahn Book 2003 Springer Science+Business Media Dordrecht 2003 Activation.Lipid.Nucleotide.cell biology.meta

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Arbeits- und OrganisationspsychologieArfs and Rac1 are discussed. A hypothesis for Arfaptin 2 as a communicator between these two small GTPases in vivo is presented. A possible role of Arfaptin 2 in Huntington’s disease is discussed. Finally, the properties of Arfophilin, which selectively binds ARFs 4, 5 and 6 are described.
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https://doi.org/10.1007/978-3-540-74705-5el eukaryotic species; including three animals, two fungi and a protist. Our analyses reveal distinct groupings of three Arf and ten Arl (Arf-like) subfamilies. These Arf and Arl subfamilies have arisen by numerous gene duplications that took place at different times during eukaryotic evolution. Som
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https://doi.org/10.1007/978-3-540-74705-5y conserved domain, the Sec7 domain, allows prediction of the number of Arf GEFs in multiple organisms and phylogenetic analyses. The profound effects of brefeldin A on membrane systems in eukaryotic cells demonstrate that its targets, the Arf GEFs, are central regulators of organelle structure and
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Arbeits- und Organisationspsychologieroteins implicated in the sorting of cargo into budding transport vesicles. Three families of large GEFs spatially and temporally regulate Arf activation in this organelle. GBF1, a BFA-resistant GEF with specificity for Class II Arfs in vitro, localizes to cis-compartments of the Golgi and appears t
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Arbeits- und Organisationspsychologietially colocalize with the Golgi 58 kDa protein and γ-adaptin, a component of the AP-1 complex. The distribution of BIG1 in the TGN is distinct from that of GBF-1, a brefeldin A (BFA)-resistant GEF that was confined to the cis-Golgi. Recently reported studies implicate BIG2 in the transport of lysos
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https://doi.org/10.1007/978-3-540-74705-5 latent GTPase activity of Arfs. The first of these to be discovered, Arf GAP1 is the focus of this chapter. It’s role in the cellular actions of Arfs, particularly vesicular traffic, and the regulation of Arf GAP1 by other factors, e.g., lipids, is discussed.
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Bettina S. Wiese,Anna M. Stertz stimulate GTP hydrolysis on all the known Arf subtypes about equally well, and this activity is stimulated by PI(3,4,5)P.. As such, GITs are negative regulators of the cellular functions of Arfs, such as intracellular vesicle traffic and cytoskeletal rearrangement. In addition, GITs form the core o
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