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RETRACTED: Molecular structure and target recognition of neuronal calcium sensor proteins

2012· article· en· 25 citations· W2065876850 on OpenAlex· 10.3389/fnmol.2012.00010

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Canadian affiliationAn author listed a Canadian institution. This is the only route the usual frame has.
Canadian funderA Canadian agency funded it. The work may carry no Canadian affiliation at all.

Post-publication record

Nature
Retraction
Reason
Duplication of/in Article;
Date
5/20/2016 0:00
Flagged by OpenAlex?
Yes

Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.

Abstract

Neuronal calcium sensor (NCS) proteins, a sub-branch of the EF-hand superfamily, are expressed in the brain and retina where they transduce calcium signals and are genetically linked to degenerative diseases. The amino acid sequences of NCS proteins are highly conserved but their physiological functions are quite distinct. Retinal recoverin and guanylate cyclase activating proteins (GCAPs) both serve as calcium sensors in retinal rod cells, neuronal frequenin (NCS1) modulates synaptic activity and neuronal secretion, K(+) channel interacting proteins (KChIPs) regulate ion channels to control neuronal excitability, and DREAM (KChIP3) is a transcriptional repressor that regulates neuronal gene expression. Here we review the molecular structures of myristoylated forms of NCS1, recoverin, and GCAP1 that all look very different, suggesting that the sequestered myristoyl group helps to refold these highly homologous proteins into very different structures. The molecular structure of NCS target complexes have been solved for recoverin bound to rhodopsin kinase (RK), NCS-1 bound to phosphatidylinositol 4-kinase, and KChIP1 bound to A-type K(+) channels. We propose that N-terminal myristoylation is critical for shaping each NCS family member into a different structure, which upon Ca(2+)-induced extrusion of the myristoyl group exposes a unique set of previously masked residues that interact with a particular physiological target.

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The record

Venue
Frontiers in Molecular Neuroscience
Topic
Retinal Development and Disorders
Field
Biochemistry, Genetics and Molecular Biology
Canadian institutions
University of TorontoOntario Institute for Cancer Research
Funders
National Eye InstituteCanadian Institutes of Health ResearchNational Institutes of Health
Keywords
RecoverinMyristoylationEF handCell biologyBiologyCalcium-binding proteinCalciumBiochemistryChemistryGeneRhodopsinPeptide sequenceRetinalPhosphorylation
Has abstract in OpenAlex
yes