Vesicle trafficking

Water soluble hormone release Transmitter release Vesicle trafficking proteins... 

SYNAPTIC VESICLE TRAFFICKING IS A SPECIALIZED FORM OF REGULATED SECRETION AND RECYCLING OPTIMIZED FOR SPEED AND EFFICIENCY 158... 

Rab is a family of small G proteins involved in membrane vesicle trafficking 343... 

Localized to synaptic vesicles, where it regulates vesicle trafficking and exocytosis... 

Rab is a family of small G proteins involved in membrane vesicle trafficking. Mammalian tissues contain around 30 forms of Rab, which specifically associate with the various types of membrane vesicles and organelles that exist in cells [30,31]. Rab proteins, named originally as ras-related proteins in brain, are isoprenylated and associate with membranes, as do isoprenylated Ras and G protein y subunits. However, unlike these other G proteins, the GTP and GDP binding to Rab appears to regulate its association with membrane compartments. 

Cholera toxin catalyzes the ADP-ribosylation of a specific arginine residue in G and Gat. This covalent modification inhibits the intrinsic GTPase activity of these a subunits and thereby freezes them in their activated, or free, state (Fig. 19-1C). By this mechanism, cholera toxin stimulates adenylyl cyclase activity and photoreceptor transduction mechanisms. The ability of cholera toxin to ADP-ribosylate G may require the presence of a distinct protein, ADP-ribosylation factor (ARF). ARF, which is itself a small G protein (Table 19-2), also is ADP-ribosylated by cholera toxin. ARF is implicated in controlling membrane vesicle trafficking (see Ch. 9). 

Blocks vesicle trafficking along microtubules lAA blocks glycolysis as well... 

An emergent field dealing with the physical/chemical processes that underlie the changes of lipid phase state during such cellular events as membrane fusion, vesicle trafficking, and cell disjunction. 

Aronin N, DiFiglia M (1992) The subcellular localization of the G-protein Gi alpha in the basal ganglia reveals its potential role in both signal transduction and vesicle trafficking. J Neurosci 12 3435—3444... 

Liu, Y., Peterson, D. A., and Schubert, D. (1998). Amyloid beta peptide alters intracellular vesicle trafficking and cholesterol homeostasis. Proc Natl Acad Sci USA 95, 13266—13271. 

In the kiss-and-run mode exocytosis and endocytosis are directly coupled to each other, while in the case of classical complete vesicle fusion, exocytosis and slow clathrin-mediated endocytosis are timely and spatially separated. However, it appears that also in the latter case exocytosis and endocytosis occur coordinated, as both are stimulated by an increase of the cytoplasmic calcium concentration. It has been shown that after calcium entry the enzyme phospho-inositol-5 kinase Iy, which is enriched in the synapse, catalyzes the synthesis of phosphatidylinos-itol (4,5)-bisphosphate and that this mechanism is important for synaptic vesicle trafficking (Di Paolo et al. 2004). As many proteins involved in clathrin-mediated endocytosis are recruited to the plasma membrane by binding to phosphatidylinosi-tol (4,5)-bisphosphate (e.g., amphiphysin, dynamin, epsin, AP-180, and AP-2) it is attractive to speculate that elevated levels of calcium mediate the recruitment of en-docytic proteins to the plasma membrane by this mechanism. The increased level of phosphatidylinositol (4,5)-bisphosphate could be in part degraded by synaptojanin that thereby initiates the disassembly of the clathrin coat. Hence, calcium-induced transient increases in the level of phosphatidylinositol (4,5)-bisphosphate appear to play a central role for coupling exocytosis to clathrin-mediated endocytosis. In addition, it has been demonstrated that calcium also leads to the dephosphorylation of endocytic proteins as amphiphysin, dynamin, and synaptojanin, which in vitro is important for efficient coat assembly (Cousin and Robinson 2001). 

Di Paolo G, Moskowitz HS, Gipson K, Wenk MR, Voronov S, Obayashi M, Flavell R, Fitzsimonds RM, Ryan TA, De Camilli P (2004) Impaired PtdIns(4,5)P2 synthesis in nerve terminals produces defects in synaptic vesicle trafficking. Nature 431 415-22 Dulubova I, Khvotchev M, Liu S, Huryeva I, Siidhof TC, Rizo J (2007) Muncl8-1 binds directly to the neuronal SNARE complex. Proc Natl Acad Sci USA. 2007 Feb 14 104, 2697-702 Edeling MA, Smith C, Owen D (2006) Life of a clathrin coat insights from clathrin and AP structures. Nat Rev Mol Cell Biol 7 32 14... 

Tang J, Maximov A, Shin OH, Dai H, Rizo J, Sudhof TC (2006) A complexin/synaptotagmin 1 switch controls fast synaptic vesicle exocytosis. Cell 126 1175-87 Toonen RF, Verhage M (2003) Vesicle trafficking pleasure and pain from SM genes. Trends Cell Biol. 13 177-86... 

Toonen RF, Verhage M (2003) Vesicle trafficking pleasure and pain from SM genes. Trends Cell Biol 13 177-86... 

VASP Regulation of actin dynamics Vesicle trafficking Aggregation of vesicle proteins Cerebellum, Hippocampus Hauser et al. 1999 Arancio et al. 2001 Wang et al. 2005... 

Septin-3 Vesicle trafficking Hippocampus COS7 cells Xue et al. 2000, 2004... 

Vesicle Trafficking and Recycling at the Neuromuscular Junction Two Pathways for Endocytosis Toshiaki Kidokoro... 

PKC is a serine/threonine protein kinase comprised of at least 11 isozymic forms (Nishizuka 1995 Liu and Heckman 1998). These isozymic forms have been classified as atypical, classical, and novel. Classical PKCs (a, pi, pH, and y) are activated by Ca2+, DAG, phosphatidylserine (PS), and the tumor promoter phorbol 12-myristate 13-acetate (PMA). Novel PKCs (6, e, r, i, and 0) are activated by DAG, PS, and unsaturated fatty acids, while atypical PKCs (C, A, and 0 are insensitive to DAG but are activated by PS and phosphatidylinositides (reviewed in Liu and Heckman 1998 Newton and Johnson 1998 Nakanishi et al. 1993). PKCs have been implicated in a wide variety of cellular responses, including growth, differentiation, gene expression, angiogenesis, contractility, and vesicle trafficking (Nishizuka 1995). 

Epithelial cells are interconnected at the apical (mucosal) side by a complex network of proteins, called the tight junctions (TJ). First thought to have merely a static role in restricting access of compounds present in the luminal fluid to the underlying subepithelial tissue and systemic circulation by the paracellular pathway, TJ are known today to be dynamic structures involved in cellular differentiation, cell signaling (Harder and Margolis 2008), polarized vesicle trafficking, and protein synthesis. 

SNARE Proteins, Vesicle Trafficking and Plant Defense... 

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