Earticle

초록

영어

Neurotransmitter release at the synapse requires the fusion of synaptic vesicles with the presynaptic plasma membrane. SNARE (soluble N-ethylmaleimide-sensitive fusion protein-attachment protein receptors) proteins mediate this synaptic fusion event, and the assembly of which to form 4-helical bundle is believed to generate the required force. SNARE complex formation is thought to be initiated at the N-terminal region and zips towards the C-terminal membrane-proximal region (a zipper model). Clostridium botulinum neurotoxins (BoNTs) elicit neuron-specific flaccid paralysis by specifically cleaving neuronal SNARE proteins. After realization of the therapeutic potentials of these otherwise fatal toxins, the controlled use of BoNT/A was approved by the FDA for the treatment of several hypersecretion-related neurological diseases such as strabismus, blepharospam, hemificial spasm and cervical dystonia. Recently, the cosmetic use of these toxins for treating glabellar facial lines and axillary hyperhidrosis has gained immense popularity. Here, we show that SNARE-driven membrane fusion, and the consequent neurotransmitter release, can be controlled by wedging the SNARE zipper with polyphenols. Polyphenols also regulated the degranulation of allergy mediators from mast cells through plopping the SNARE zippers in mast cells. Polyphenols were specific to SNARE complexes. In conclusion, some polyphenols behave like “plant-derived small molecule Botox.”

저자

• Yoosoo Yang [ Department of Genetic Engineering, Sungkyunkwan University, Suwon, Gyeonggi-do 440-746, South Korea, Biomedical Research Institute, Korea Institute of Science and Technology Seoul, Korea ]
• Dae-Hyuk Kweon [ Department of Genetic Engineering, Sungkyunkwan University, Suwon, Gyeonggi-do 440-746, South Korea ]

참고문헌

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간행물

표지보기 관심저널 등록

• 간행물명

  한국생물공학회 학술대회

• 간기

  반년간

• 수록기간

  1985~2013

• 십진분류

  KDC 476 DDC 576