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Vesicle trafficking with snares: a perspective for autism

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Date

2022

Author

Özdemir, Çilem
Şahin, Nilfer
Edgünlü, Tuba

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Citation

Özdemir, Ç., Şahin, N. & Edgünlü, T. Vesicle trafficking with snares: a perspective for autism. Mol Biol Rep (2022). https://doi.org/10.1007/s11033-022-07970-5

Abstract

Vesicle-mediated membrane traffic is the mechanism fundamental to many biological events, especially the release of neurotransmitters. The main proteins of the mechanism that mediates membrane fusion in vesicle-mediated membrane traffic are N-ethylmaleimide sensitive factor (NSF) supplemental protein (SNAP) receptor (SNAREs) proteins. SNAREs are classified into vesicle-associated SNAREs (vesicle-SNAREs/v-SNAREs) and target membrane-associated SNAREs (target-SNARE/t-SNAREs). Autism spectrum disorders (ASD) are neurodevelopmental disorders characterized by many symptoms, especially complications in social communication and stereotypical behaviours. Defects in synaptogenesis and neurotransmission, oxidative stress, and developmental defects in the early stages of development are defined in the pathogenesis of the disease. SNARE proteins are on the basis of synaptogenesis and neurotransmission. Although the formation mechanisms and underlying causes of the SNARE complex are not fully understood, expression differences, polymorphisms, abnormal expressions or dysfunctions of the proteins that make up the SNARE complex have been associated with many neurodevelopmental diseases, including autism. Further understanding of SNARE mechanisms is crucial both for understanding ASD and for developing new treatments. In this review, the formation mechanisms of the SNARE complex and the roles of various factors involved in this process are explained. In addition, a brief evaluation of clinical and basic studies on the SNARE complex in autism spectrum disorders was made.

Source

Molecular Biology Reports

URI

https://doi.org/10.1007/s11033-022-07970-5
https://hdl.handle.net/20.500.12809/10351

Collections

  • Dahili Tıp Bilimleri Bölümü Koleksiyonu [691]
  • PubMed İndeksli Yayınlar Koleksiyonu [2082]
  • Scopus İndeksli Yayınlar Koleksiyonu [6219]



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