SNAP-25, a SNARE protein, inhibits two types of K+ channels in esophageal smooth muscle

Ji, Junzhi; Salapatek, Anne Marie; Lau, Helena; Wang, Guotang; Gaisano, Herbert Y.; Diamant, Nicholas E.

doi:10.1053/gast.2002.32412

Cited by 32 publications

(33 citation statements)

References 28 publications

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“…Besides its role on neurotransmitter release, SNAP-25 modulates the activity of Ca 2+ channels and possibly other voltage gated ion channels (He et al, 2008;Ji et al, 2002;Pozzi et al, 2007;Zamponi, 2003). By targeting SNAP-25, BoNT/A may prevent the SNAREmediated translocation of receptors to plasma membrane, such as N-methy-D-aspartate receptor and transient receptor potential vanilloid 1 (TRPV1) MorenillaPalao et al, 2004;Shimizu et al, 2012).…”

Section: Additional Actions Of Bont/a Mediated By Snap-25mentioning

confidence: 99%

Botulinum toxin A, brain and pain

Matak

Lacković

2014

Progress in Neurobiology

143

114

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Section: Additional Actions Of Bont/a Mediated By Snap-25mentioning

confidence: 99%

Botulinum toxin A, brain and pain

Matak

Lacković

2014

Progress in Neurobiology

143

114

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“…This interaction is likely of little relevance to insulin secretion as Kv1.1 is not expressed in rat or human islets (Table 2) and the Kv1.1 inhibitor dendrotoxin has little effect on insulin secretion and outward currents, even in the same HIT-T15 cell line [52]. In oesophageal smooth muscle cells, SNAP-25 was found to inhibit both Kv and K Ca currents, causing a leftward shift of voltage-dependent activation of K Ca but not Kv channels [135]. The molecular correlates of these currents were not identified in this study.…”

Section: Regulation Of Kv Channel Activity In Beta Cellsmentioning

confidence: 99%

Voltage-dependent K + channels in pancreatic beta cells: Role, regulation and potential as therapeutic targets

2003

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Insulin secretion from pancreatic islet beta cells is acutely regulated by a complex interplay of metabolic and electrogenic events. The electrogenic mechanism regulating insulin secretion from beta cells is commonly referred to as the ATP-sensitive K + (K ATP ) channel dependent pathway. Briefly, an increase in ATP and, perhaps more importantly, a decrease in ADP stimulated by glucose metabolism depolarises the beta cell by closing K ATP channels. Membrane depolarisation results in the opening of voltage-dependent Ca 2+ channels, and influx of Ca 2+ is the main trigger for insulin secretion. Repolarisation of pancreatic beta cell action potential is mediated by the activation of voltage-dependent K + (Kv) channels. Various Kv channel homologues have been detected in insulin secreting cells, and recent studies have shown a role for specific Kv channels as modulators of insulin secretion. Here we review the evidence supporting a role for Kv channels in the regulation of insulin secretion and discuss the potential and the limitations for beta-cell Kv channels as therapeutic targets. Furthermore, we review recent investigations of mechanisms regulating Kv channels in beta cells, which suggest that Kv channels are active participants in the regulation of beta-cell electrical activity and insulin secretion. [Diabetologia (2003[Diabetologia ( ) 46:1046[Diabetologia ( -1062

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“…This observation suggests regional specialization for these SNARE proteins, which in turn may provide functional specificity for the ubiquitously expressed VAP-A. Specific SNARE proteins found within esophageal smooth muscle have been shown to modulate membrane excitability and contractility in SMCs by regulating Kϩ membrane ion channels (Ji et al, 2002b). In addition, it has been suggested that the intrinsic conductive properties of SMCs are associated with specific SNARE protein expression (Salapatek and Dia- mant, 1998; Ji et al, 2002a;Salapatek et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Vesicle‐associated protein‐A is differentially expressed during intestinal smooth muscle cell differentiation

Gabetta

Trzyna

Phiel

et al. 2003

Developmental Dynamics

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Gastrointestinal (GI) smooth muscle diseases represent a major health concern affecting in excess of 2 million people each year. Little is currently known regarding the molecular mechanisms controlling either normal or pathogenic GI smooth muscle development. In an effort to identify the specific gene products responsible for modulating GI smooth muscle cell (SMC) differentiation, we performed differential display on distinct intestinal SMC (ISMC) phenotypes. This analysis identified over 40 unique transcripts that appeared to be differentially expressed in distinct SMC phenotypes. One such transcript that appeared to be preferentially expressed in immature smooth muscle myocytes was identified as vesicle-associated membrane protein, associated protein A (VAP-A). Northern blot analysis confirmed that VAP-A was expressed threefold higher in immature smooth muscle myocytes when compared with both smooth muscle myoblasts and mature smooth muscle myocytes. VAP-A mRNA was differentially expressed during normal rat development and showed peak levels of expression in the intestine during late embryogenesis and early neonatal development. These observations provide the first evidence that VAP-A-mediated membrane trafficking may play an important role in modulating ISMC differentiation. Developmental Dynamics 228:11-20, 2003.

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SNAP-25, a SNARE protein, inhibits two types of K+ channels in esophageal smooth muscle

Cited by 32 publications

References 28 publications

Botulinum toxin A, brain and pain

Botulinum toxin A, brain and pain

Voltage-dependent K + channels in pancreatic beta cells: Role, regulation and potential as therapeutic targets

Vesicle‐associated protein‐A is differentially expressed during intestinal smooth muscle cell differentiation

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