Disease relevance of Transport Vesicles

• Further, VCP is the mammalian homologue of yeast Cdc48p (ref. 3) and is a member of a larger gene family that includes putative ATP-binding proteins involved in vesicle transport and fusion, 26S proteasome function, regulation of the expression of human immunodeficiency virus, and assembly of peroxisomes [1].
• In summary, our data suggest that GABARAP acts via a vesicle transport mechanism as a tumor suppressor in breast cancer [2].
• Consistent with a lipid trafficking defect, Tangier disease late endocytic vesicles accumulated both cholesterol and sphingomyelin and were immobilized in a perinuclear localization [3].
• Additionally, we show that BK and NS-1619 significantly increased the density of transport vesicles in the cytoplasm of brain tumor capillary endothelia and tumor cells [4].
• These results will help to elucidate the association of upregulation of vesicle transport systems including ARF4L and stress responses of neurons after transient ischemia [5].

Psychiatry related information on Transport Vesicles

• We hypothesize that Alzheimer's disease is caused by free radical damage to membranes of endocytic vesicles due to defective binding of iron and aluminium by Tf C2 [6].

High impact information on Transport Vesicles

• In this issue of Cell, provide intriguing evidence for a new pathway that links polarity proteins and vesicle transport to the maintenance of tight junctions, through the control of Cdc42 by Rich1, a GTPase-activating protein [7].
• These data suggest that TIP47 binds MPR cytoplasmic domains and facilitates their collection into transport vesicles destined for the Golgi [8].
• Sec6/8 complex is recruited to cell-cell contacts and specifies transport vesicle delivery to the basal-lateral membrane in epithelial cells [9].
• One of the two minor targets of NEM is GM130, previously implicated in the docking of transport vesicles and mitotic fragmentation of the Golgi stack [10].
• Protein interactions regulating vesicle transport between the endoplasmic reticulum and Golgi apparatus in mammalian cells [11].

Chemical compound and disease context of Transport Vesicles

• Thus adaptational changes including mucosal hyperplasia and the appearance of two sodium-dependent D-glucose brush-border membrane vesicle transport systems occur in the residual distal intestine after massive proximal small bowel resection [12].

Biological context of Transport Vesicles

• The Rab family of low-molecular-mass GTP-binding proteins are thought to guide membrane fusion between a transport vesicle and the target membrane, and to determine the specificity of docking [13].
• Inhibition was greater than or equal to 90% when the added cdc2 activity was in the range estimated for that in mitotic Xenopus eggs, which indicates that during mitosis the cdc2 kinase mediates an inhibition of endocytic vesicle fusion, and possibly other fusion events in membrane traffic [14].
• All vesicle transport steps also have an essential requirement for a member of the Sec1 protein family, including the neuronal Munc18-1 (also known as nSec1) in regulated exocytosis [15].
• Members of the kinesin superfamily of motor proteins are essential for mitotic and meiotic spindle organization, chromosome segregation, organelle and vesicle transport, and many other processes that require microtubule-based transport [16].
• The Cdc42 GTPase binds to numerous effector proteins that control cell polarity, cytoskeletal remodelling and vesicle transport [17].

Anatomical context of Transport Vesicles

• CLIP-170 links endocytic vesicles to microtubules [18].
• Ultra-structural localization studies demonstrate that colloidal gold-alpha 2M is found predominantly in endocytic vesicles, while ferritin-transferrin is found in small vesicles and tubular structures in a region adjacent to the Golgi complex [19].
• We conclude that negatively charged liposomes are endocytosed and processed intracellularly by the coated vesicle pathway, and acidification of the endocytic vesicle, rather than liposome fusion, permits escape of certain molecules to the cytoplasm [20].
• To fuse transport vesicles with target membranes, proteins of the SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) complex must be located on both the vesicle (v-SNARE) and the target membrane (t-SNARE) [21].
• A protein sensitive to N-ethylmaleimide catalyses the fusion of transport vesicles with Golgi cisternae in a mammalian cell-free system [22].

Associations of Transport Vesicles with chemical compounds

• Interestingly, while the earliest steps in stack formation share some similarities with events catalyzing fusion of transport vesicles to its target membrane, neither GTP gamma S nor Rab-GDI, inhibitors of vesicular protein traffic, inhibit stack formation [23].
• Role of an N-ethylmaleimide-sensitive transport component in promoting fusion of transport vesicles with cisternae of the Golgi stack [24].
• To measure chloride transport, endocytic vesicles were labelled in vivo with a Cl(-)-sensitive fluorescent indicator6-8 [25].
• SEC12 encodes a guanine-nucleotide-exchange factor essential for transport vesicle budding from the ER [26].
• The effects of AMP-PNP on the vesicle transport system indicate that the enzymatic machinery of this system differs significantly from that of the actomyosin system or the dynein-microtubule system [27].

Gene context of Transport Vesicles

• The functional interactions of Bos1p with Ypt1p and Sec22p may be necessary for the fusion competence of the ER to Golgi transport vesicles [28].
• We cloned opb by a map-based approach and found that it encodes Rab23, a member of the Rab family of vesicle transport proteins [29].
• In rme-6 mutants, transport from the plasma membrane to endosomes is defective, and small 110-nm endocytic vesicles accumulate just below the plasma membrane [30].
• Sec12p-dependent membrane binding of the small GTP-binding protein Sar1p promotes formation of transport vesicles from the ER [31].
• These findings indicate that Sec16p associates with Sec23p as part of the transport vesicle coat structure [32].

Analytical, diagnostic and therapeutic context of Transport Vesicles

• Immunoelectron microscopy showed that the 180/90-kDa glycoprotein was localized in coated pits of the cell surface and in intracellular endocytic vesicles (receptosomes/endosomes) [33].
• Munc-18b had a similar distribution to Munc-18c and so may also be involved in vesicle transport to the cell surface, whereas Munc-18a was undetectable by immunoblotting in adipocytes [34].
• Furthermore, confocal laser scanning microscopy showed that cofilin existed diffusely in the cytosol and nuclear region of the resting cells, while in the activated cells, it was accumulated at the plasma membrane area, forming ruffles or endocytic vesicles on which O2.- should be produced [35].
• Double label indirect immunofluorescence in cells and immunoblotting of immunoisolated tubular networks revealed that proteins involved in formation of ER-derived transport vesicles, namely p58/ERGIC 53, Sec23p, and Sec13p, were concentrated in the E1-containing pre-Golgi compartment [36].
• Screening for proteins by immunofluorescence microscopy revealed that the small G protein, Rab4, was associated with 80% of hepatocyte-derived early endocytic vesicles that contain the ligand asialoorosomucoid (ASOR) [37].

References