Allostery and instability in the functional plasticity of synaptotagmin I

Synaptotagmin I (Syt I) is the calcium ion sensor for regulated release of neurotransmitter. How Syt I mediates this cellular event has been a question of extensive study for decades and yet, a clear understanding of the protein’s diverse functionality has remained elusive. Using tools of thermodyna...

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Main Authors: Fealey, Michael E., Hinderliter, Anne
Format: Online
Language:English
Published: Landes Bioscience 2013
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3609835/
id pubmed-3609835
recordtype oai_dc
spelling pubmed-36098352013-06-07 Allostery and instability in the functional plasticity of synaptotagmin I Fealey, Michael E. Hinderliter, Anne Article Addendum Synaptotagmin I (Syt I) is the calcium ion sensor for regulated release of neurotransmitter. How Syt I mediates this cellular event has been a question of extensive study for decades and yet, a clear understanding of the protein’s diverse functionality has remained elusive. Using tools of thermodynamics, we have identified two intrinsic properties that may account for Syt I’s functional plasticity: marginal stability and negative coupling. These two intrinsic properties have the potential to provide great conformational flexibility and suggest that Syt I’s functional plasticity stems in part from subtle rearrangements in the protein’s conformational ensemble. This model for Syt I function is discussed within the context of the nervous system’s overall plasticity. Landes Bioscience 2013-03-01 2013-03-01 /pmc/articles/PMC3609835/ /pubmed/23750295 http://dx.doi.org/10.4161/cib.22830 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Fealey, Michael E.
Hinderliter, Anne
spellingShingle Fealey, Michael E.
Hinderliter, Anne
Allostery and instability in the functional plasticity of synaptotagmin I
author_facet Fealey, Michael E.
Hinderliter, Anne
author_sort Fealey, Michael E.
title Allostery and instability in the functional plasticity of synaptotagmin I
title_short Allostery and instability in the functional plasticity of synaptotagmin I
title_full Allostery and instability in the functional plasticity of synaptotagmin I
title_fullStr Allostery and instability in the functional plasticity of synaptotagmin I
title_full_unstemmed Allostery and instability in the functional plasticity of synaptotagmin I
title_sort allostery and instability in the functional plasticity of synaptotagmin i
description Synaptotagmin I (Syt I) is the calcium ion sensor for regulated release of neurotransmitter. How Syt I mediates this cellular event has been a question of extensive study for decades and yet, a clear understanding of the protein’s diverse functionality has remained elusive. Using tools of thermodynamics, we have identified two intrinsic properties that may account for Syt I’s functional plasticity: marginal stability and negative coupling. These two intrinsic properties have the potential to provide great conformational flexibility and suggest that Syt I’s functional plasticity stems in part from subtle rearrangements in the protein’s conformational ensemble. This model for Syt I function is discussed within the context of the nervous system’s overall plasticity.
publisher Landes Bioscience
publishDate 2013
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3609835/
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