High impact information on VAMP4

• Reducing GGA3 levels by using short interfering (si)RNA also led to VAMP4 retention in SGs, and inhibition of PC2 activity [1].
• We demonstrate that fusion is largely mediated by a complex formed by syntaxin 13, syntaxin 6, vti1a, and VAMP4, whereas the exocytic and late endosomal SNAREs play little or no role in the reaction [2].
• When C-terminally tagged with enhanced green fluorescent protein, the majority of Vamp4 and Vamp5 is correctly targeted to the TGN and plasma membrane, respectively [3].
• Indirect immunofluorescence and electron microscopy revealed that the majority of VAMP4 localized to tubular and vesicular membranes of the TGN, which were in part coated with clathrin [4].
• Vesicle-associated membrane protein 4 is implicated in trans-Golgi network vesicle trafficking [4].

Biological context of VAMP4

• Suicide attempt and basic mechanisms in neural conduction: relationships to the SCN8A and VAMP4 genes [5].

Anatomical context of VAMP4

• Both proteins had a distinct but overlapping localization. vtila was found predominantly on the Golgi and the TGN, vtilb mostly on tubules and vesicles in the TGN area and on endosomes. vti1a coimmunoprecipitated with VAMP-4, syntaxin 6, and syntaxin 16 [6].
• VAMP4 is expressed in liver and skeletal muscle and participates in intracellular trafficking of secreted and membrane-associated proteins [7].

Associations of VAMP4 with chemical compounds

• AP-1 association with VAMP4 is enhanced when serine 30, in an acidic cluster, is phosphorylated by casein kinase 2 [8].

Physical interactions of VAMP4

• Immunoprecipitation of VAMP4 from rat brain detergent extracts revealed that VAMP4 exists in a complex containing syntaxin 6 [4].
• AP-1 recruitment to VAMP4 is modulated by phosphorylation-dependent binding of PACS-1 [8].

Co-localisations of VAMP4

• In these compartments, VAMP4 was found to colocalize with the putative TGN-trafficking protein syntaxin 6 [4].

Other interactions of VAMP4

• A dominant-negative PACS-1, which binds acidic clusters but not AP-1, also causes mislocalization of VAMP4 [8].
• Replication in a separate sample, consisting of 190 triplets, confirmed the exploratory data for the SCN8A (P = 0.005) and VAMP4 (P = 0.019) genes, but failed to confirm the data for the RABAC1 gene [5].
• Two SNAREs, VAMP4 and synaptotagmin IV, enter newly formed granules but are removed from the maturing granule membrane by vesicle budding [9].

References