Disease relevance of STXBP2

• Overexpression of the wild-type Munc18-2 was shown to inhibit the apical delivery of influenza virus hemagglutinin (HA) [1].

High impact information on STXBP2

• Even the Munc18-2 mutants that do not detectably bind syntaxin 3 were membrane associated in Caco-2 cells, suggesting that the syntaxin interaction is not the sole determinant of Sec1 protein membrane attachment [1].
• These findings suggest a role for Munc18-2 and the microtubule network in the regulation of secretory granule dynamics in mast cells [2].
• Disruption of the microtubule network with nocodazole provoked Munc18-2 redistribution and affected mediator release [2].
• Munc18-2 localisation on granules is polarised; however, upon stimulation Munc18-2 redistributed into forming lamellipodia and persisted on granules that were aligned along microtubules, but was excluded from F-actin ruffles [2].
• Furthermore, overexpression of the ubiquitous isoform of munc-18, munc-18-2, is also capable of rescuing the transport of the t-SNARE [3].

Biological context of STXBP2

• Evidence of a role for Munc18-2 and microtubules in mast cell granule exocytosis [2].
• The Munc18-2 gene comprises 19 exons whose sizes range from 50 to 158 bp, with a total gene size of approximately 11 kb [4].
• Analysis of the region upstream of the transcription start site shows that Munc18-2 has a TATA-less promoter, with a consensus initiator (Inr) sequence at the start of transcription, several Sp1 binding sites, and strong promoter activity in RBL-2H3 mast cells [4].

Anatomical context of STXBP2

• Munc-18-2, a member of this family, is predominantly expressed in the epithelial cells of several tissues [5].
• We demonstrate here that Munc-18-2 colocalizes with syntaxin 3 at the apical plasma membrane of intestinal epithelium and Caco-2 cells [5].

Associations of STXBP2 with chemical compounds

• The amount of Munc-18-2 in the complex increases upon treatment of the cells with the protein kinase C activator phorbol myristate acetate, indicating a functional connection between the complex and cell signalling [5].
• The quantity of the complex is reduced by treatment of Caco-2 cells with the alkylating agent N-ethylmaleimide which also has an inhibitory effect on the ability of Munc-18-2 to associate with syntaxin 3 in vitro [5].

References