2011
DOI: 10.1091/mbc.e11-02-0135
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Munc18-1 domain-1 controls vesicle docking and secretion by interacting with syntaxin-1 and chaperoning it to the plasma membrane

Abstract: Striking correlations exist between the abilities of domain-1 cleft mutants of Munc18-1 to bind and chaperone syntaxin-1 and their ability to restore vesicle docking and secretion.

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Cited by 56 publications
(78 citation statements)
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References 59 publications
(122 reference statements)
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“…4). This same cavity has been implicated in the binding of SNARE complexes (24,26,27). The Munc18 binding site of the Sx H3 helix is not definitive in our model; indeed, it is likely to be very flexible.…”
Section: Discussionmentioning
confidence: 66%
See 1 more Smart Citation
“…4). This same cavity has been implicated in the binding of SNARE complexes (24,26,27). The Munc18 binding site of the Sx H3 helix is not definitive in our model; indeed, it is likely to be very flexible.…”
Section: Discussionmentioning
confidence: 66%
“…Rathore et al showed that the Sx Npeptide recruits Munc18-1 for assembly of the SNARE:SM complex and does not need to be attached to Sx to exert this effect (25). Finally, the central cavity of the SM protein has been linked to binding of closed Sx1a and to binding of the core helical bundle of SNARE complexes (24,26,27).…”
mentioning
confidence: 99%
“…We previously found that Munc18-1/2 DKD causes not only a strong reduction in syntaxin-1 level but also perturbation of its plasmalemmal localization in PC12 cells (15,16). We therefore examined whether the subcellular localization of syntaxin-11 can be significantly altered by Munc18-1/2 DKD in RBL-2H3 cells ( Fig.…”
Section: Resultsmentioning
confidence: 97%
“…The Munc18 family of proteins has been revealed to play multiple functions, which include both chaperoning cognate syntaxins (14)(15)(16)(17)(18)(19) and priming/stimulating membrane fusion through interaction with the SNARE complex (20-23) (reviewed in ref. 24).…”
mentioning
confidence: 99%
“…To examine whether the reduction in fusion events resulted from reduced SV docking in response to stimulation, we used PC12 cells engineered to knock down Munc18-1 and Munc18-2 (DKD-PC12 cells) 31 , which have been shown to exhibit defective vesicle docking 31,33 . Electron microscopy analysis revealed that the number of predocked granules in these cells was significantly reduced in comparison with that in DKD-PC12 cells in which wild-type Munc18-1 (Munc18-1) expression was rescued (Fig.…”
Section: Svs and Cortical Actin Approach The Plasmalemma On Stimulationmentioning
confidence: 99%