High impact information on Stx3

• Syntaxin-3 and syntaxin-1A inhibit L-type calcium channel activity, insulin biosynthesis and exocytosis in beta-cell lines [1].
• We compared this with the expression patterns of syntaxin 1A, 2, 3, 4, and 5, and found that syntaxin 3 was enriched in the same epithelial structures in which Munc-18-2 was abundant [2].
• Syntaxin 3 and Munc-18-2 in epithelial cells during kidney development [2].
• This was in marked contrast to another type II membrane protein (syntaxin 3) that rapidly defaulted to the plasma membrane 3 h after expression [3].
• Furthermore, truncation of the syntaxin 3 transmembrane domain to 17 amino acids resulted in a complete conversion to cis-Golgi compartmentalization that was indistinguishable from syntaxin 5 [4].

Biological context of Stx3

• These forms of syntaxin 3 are probably generated by alternative splicing of the primary transcript of syntaxin 3 gene [5].
• cDNAs for four different forms of syntaxin 3 were cloned from a mouse brain cDNA library, and the proteins encoded by these clones were named syntaxin 3A (previous syntaxin 3), 3B, 3C and 3D [5].

Anatomical context of Stx3

• We summarize here data on the presence and the functional role of vesicle transport proteins in the kidney, and describe work addressing the developmentally regulated expression and localization of three molecules suggested to be involved in polarized trafficking in kidney epithelia, Rab17, syntaxin 3, and Munc-18-2 [6].
• Syntaxin 3 was found in glutamatergic photoreceptor and bipolar cell ribbon synapses, but was absent from putative conventional glutamatergic amacrine cell synapses [7].

Analytical, diagnostic and therapeutic context of Stx3

• METHODS: Expression patterns were studied by in situ hybridization and immunocytochemistry and the complex formation of syntaxin 3 and Munc-18-2 by coimmunoprecipitation and Western blotting [2].

References