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1 t have a unique and specific requirement for complexin I.
5 cies now show that the region containing the Complexin-I accessory helix and preceding N-terminal seq
7 ing or decreasing the negative charge of the complexin-I accessory helix inhibits or stimulates relea
10 n the observation of simultaneous binding of complexin-I and a fragment containing the synaptotagmin-
14 Sperm are unusual because they express both complexins I and II but have a unique and specific requi
17 In the recently solved crystal structure of complexin I bound to the synaptic SNARE complex, complex
18 data on mice, with predominant expression of complexin I by inhibitory neurons, and complexin II by e
23 omplexin-I inhibitory helix without inducing complexin-I dissociation, thus relieving the inhibitory
24 sical techniques, here we show that C2AB and complexin-I do not bind to each other but can indeed bin
26 nd/or phospholipids increase the affinity of complexin-I for the SNARE complex, hindering dissociatio
28 py experiments show that C2AB can displace a complexin-I fragment containing its central SNARE-bindin
30 tron microscopy demonstrated the presence of complexin I/II in horizontal cell processes postsynaptic
33 the cellular and subcellular distribution of complexin I/II, syntaxin-1, and synapsin I in rabbit ret
37 mp' mutations that enhanced or decreased the complexin-I inhibitory activity in cell-cell fusion assa
38 or indirectly causes a rearrangement of the complexin-I inhibitory helix without inducing complexin-
39 suggested that an 'accessory' alpha-helix of Complexin-I inhibits release by inserting into the C-ter
44 The membrane-proximal accessory helix of complexin is necessary for clamping, but its mechanism o
45 racterized the minimal functional domains of complexin-I necessary to couple calcium and synaptotagmi
46 n vivo experiments postulate that domains of complexin-I produce different effects on neurotransmitte
48 For both mRNA and protein, the complexin II/complexin I ratio was lower in schizophrenia, confirming
50 f N-terminal and central domain fragments of complexin is sufficient to activate Ca(2+)-triggered rel
52 These data suggest that the main function of complexin is to maintain the docked state both by inhibi
53 her with NMR data, suggests that the role of complexin is to stabilize the SNARE complex as it forms
54 actions of N- and/or C-terminal sequences of complexin-I with the SNARE complex and/or phospholipids
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