Synaptosomal-associated protein 25

Synaptosomal-associated protein, 25kDa
PDB rendering based on 1jth.
Available structures
PDB Ortholog search: RCSB
Identifiers
SNAP25 Gene
RNA expression pattern

Synaptosomal-associated protein 25 (SNAP-25) is a t-SNARE protein that is encoded by the SNAP25 gene in humans.[1] SNAP-25 is a component of the trans-SNARE complex, which is proposed to account for the specificity of membrane fusion and to directly execute fusion by forming a tight complex that brings the synaptic vesicle and plasma membranes together.[2]

Structure and function

SNAP-25 is a membrane bound protein anchored to the cytosolic face of membranes via palmitoyl side chains in the middle of the molecule. SNAP-25 is a Q-SNARE protein contributing two α-helices in the formation of the exocytotic fusion complex in neurons where it assembles with syntaxin-1 and synaptobrevin. SNAP-25 inhibits P/Q- and L-type voltage-gated calcium channels located presynaptically[3] and interacts with the synaptotagmin C2B domain in Ca2+-independent fashion.[4] In glutamatergic synapses SNAP-25 decreases the Ca2+ responsiveness, while it is naturally absent in GABAergic synapses.[5]

SNAP-25 family
Structure of a SNARE complex involved in synaptic exocytosis.
Identifiers
Symbol SNAP-25
Pfam InterPro IPR000928
SCOP SUPERFAMILY 1sfc

Clinical significance

Consistent with the regulation of synaptic Ca2+ responsiveness, heterozygous deletion of the SNAP-25 gene in mice results in a hyperactive phenotype similar to attention deficit hyperactivity disorder (ADHD). In heterozygous mice, a decrease in hyperactivity is observed with dextroamphetamine (or Dexedrine), an active ingredient in the ADHD drug Adderall. Homozygous deletions of the SNAP-25 gene are lethal. Subsequent studies have suggested that at least some of the SNAP-25 gene mutations in humans might predispose to ADHD.[7][8]

A genome wide association study pointed to the rs362584 polymorphism in the gene as possibly associated with the personality trait neuroticism.[9] Botulinum toxins A, C and E cleave SNAP-25[10] leading to paralysis in clinically developed botulism.

Interactive pathway map

Click on genes, proteins and metabolites below to link to respective articles. [§ 1]

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Interactions

SNAP-25 has been shown to interact with STX4,[11][12][13][14] STX2,[11][12] Syntaxin 3,[11][12][14] STX1A,[11][12][14][15][16][17][18][19][20][21][22] KIF5B,[23] TRIM9,[20] STX11,[15][24] CPLX1,[22][25] SYT1,[26][27] VAMP2,[20][22][28] SNAPAP[19] and ITSN1.[29]

References

Further reading

External links

  • Medical Subject Headings (MeSH)


This article incorporates text from the IPR000928