Vesicle Transport through Interaction with T-SNAREs Homolog 1B (Yeast) Proteine (VTI1B)

Human Vesicle Transport through Interaction with T-SNAREs Homolog 1B (Yeast) (VTI1B) Interaktionspartner

1. RABGEF1 mediates recycling endosome fusion with GAS-containing autophagosome-like vacuoles through the STX6-VAMP3-VTI1B complex; SNAREs are involved in autophagosome formation in response to bacterial infection

2. Vti1b-dependent tethering of Lytic granule and CD3-endo determines accumulation, docking, and efficient lytic granule secretion at the immunological synapse.

3. Results suggest that the combinational SNARE proteins VAMP8 and Vti1b mediate the fusion of antimicrobial and canonical autophagosomes with lysosomes, an essential event for autophagic degradation.

4. A dual mechanism controlling the localization and function of exocytic v-SNAREs.

5. Ca(2+) dissociates the Hrs-containing complex but not the VAMP-2-containing SNARE complex

6. epsin 4 epsin-related protein is an adaptor for vti1b

7. Results report that syntaxin 7, syntaxin 8, vti1b and VAMP8 physically and functionally interact with CFTR.

Mouse (Murine) Vesicle Transport through Interaction with T-SNAREs Homolog 1B (Yeast) (VTI1B) Interaktionspartner

1. This studied demonstratedt that the dominant negative SNARE (dnSNARE) mouse model to dissect the role of astrocyte-derived signaling in corticolimbic circuits, with implications for cognitive processing. We found that the blockade of gliotransmitter release in astrocytes triggers a critical desynchronization of neural theta oscillations between dorsal hippocampus and prefrontal cortex.

2. Our data demonstrate that contrary to the accepted model, SEC22B is not necessary for cross-presentation, cautioning against extrapolating phenotypes from knockdown studies alone.

3. This study reveals that the SNARE-dependent exocytosis in glial cells contributes to neurotoxicity during ischemia in vivo and suggests glial exocytosis as a target for therapeutic approaches.

4. syntaxin 1 and vesicle-associated membrane protein 1 are more suitable targets to abolish functional soluble N-ethylmaleimide-sensitive factor attachment protein receptor complexes

5. The dnSNARE mice performed significantly better than littermate controls on rung walk and adhesive dot removal tasks following lesion. and demonistraed that the important role of astrocytic signaling under ischemic conditions.

6. These results suggest that SNARE proteins are necessary for the increased activity of KCC2 after Zn(2+) stimulation of mZnR/GPR39.

7. Results suggest that by regulating the availability of Vti1b, Stx11 regulates trafficking steps between late endosomes, lysosomes and the cell surface in macrophages.

8. The identify IR as the first known tyrosine kinase for Munc18c as in GLUT4 vesicle exocytosis, exemplifying a new model for the coordination of SNARE assembly and vesicle mobilization events in response to a single extracellular stimulus.

9. Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development

10. Data show that deletion of CSPalpha produces an abnormal SNAP-25 conformer that inhibits SNARE-complex formation, and is subject to ubiquitylation and proteasomal degradation.

11. Lysosomal fusion and SNARE function are impaired by cholesterol accumulation in lysosomal storage disorders.

12. Data identified a number of novel synaptic protein interactions involving soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs), calcium-activated potassium channel (BKCa) alpha subunits, and dynamin-1.

13. Crystal structure of the endosomal SNARE complex reveals common structural principles of all SNAREs

14. vti1b has a role in binding to syntaxin 8

15. Syntaxin 6 and Vti1b form a SNARE complex, which is up-regulated in activated macrophages to facilitate exocytosis of tumor necrosis Factor-alpha

16. characterization of the molecular details governing the sorting of a SNARE into clathrin-coated vesicles, namely the direct recognition of the three-helical bundle H(abc) domain of the mouse SNARE Vti1b by the human clathrin adaptor epsinR