Role of tau N-terminal motif in the secretion of human tau by End Binding proteins.
Amino Acid Motifs
Amino Acid Sequence
Animals
Binding Sites
/ genetics
COS Cells
Chlorocebus aethiops
Chromatography, Affinity
Humans
Mice
Mice, Transgenic
Microtubule-Associated Proteins
/ genetics
Protein Binding
Recombinant Proteins
/ chemistry
Sequence Deletion
Species Specificity
tau Proteins
/ chemistry
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2019
2019
Historique:
received:
28
05
2018
accepted:
03
01
2019
entrez:
23
1
2019
pubmed:
23
1
2019
medline:
23
10
2019
Statut:
epublish
Résumé
For unknown reasons, humans appear to be particular susceptible to developing tau pathology leading to neurodegeneration. Transgenic mice are still undoubtedly the most popular and extensively used animal models for studying Alzheimer's disease and other tauopathies. While these murine models generally overexpress human tau in the mouse brain or specific brain regions, there are differences between endogenous mouse tau and human tau protein. Among them, a main difference between human and mouse tau is the presence of a short motif spanning residues 18 to 28 in the human tau protein that is missing in murine tau, and which could be at least partially responsible for that different susceptibility across species. Here we report novel data using affinity chromatography analysis indicating that the sequence containing human tau residues 18 to 28 acts a binding motif for End Binding proteins and that this interaction could facilitate tau secretion to the extracellular space.
Identifiants
pubmed: 30668577
doi: 10.1371/journal.pone.0210864
pii: PONE-D-18-15986
pmc: PMC6342323
doi:
Substances chimiques
MAPRE1 protein, human
0
MAPRE3 protein, human
0
MAPT protein, human
0
Mapt protein, mouse
0
Microtubule-Associated Proteins
0
Recombinant Proteins
0
tau Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0210864Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
Références
Proc Natl Acad Sci U S A. 2011 May 24;108(21):8826-31
pubmed: 21551097
Nat Cell Biol. 2009 Jul;11(7):909-13
pubmed: 19503072
Mol Cell Biochem. 1994 Jan 26;130(2):187-96
pubmed: 8028597
Nat Cell Biol. 2008 Oct;10(10):1181-9
pubmed: 18806788
FEBS Lett. 2006 Sep 4;580(20):4842-50
pubmed: 16914144
Biochemistry. 2001 May 22;40(20):5983-91
pubmed: 11352733
J Cell Biol. 2002 Nov 25;159(4):589-99
pubmed: 12446741
Mol Biol Cell. 2016 Oct 1;27(19):2924-34
pubmed: 27466319
Int J Dev Biol. 1994 Mar;38(1):13-25
pubmed: 8074993
J Neurosci. 2017 Nov 22;37(47):11406-11423
pubmed: 29054878
Cell Mol Life Sci. 2016 May;73(10):2053-77
pubmed: 26969328
Proc Natl Acad Sci U S A. 1988 Jun;85(11):4051-5
pubmed: 3131773
J Neurochem. 2015 Jun;133(5):653-67
pubmed: 25761518
Acta Neuropathol. 1991;82(4):239-59
pubmed: 1759558
J Neurochem. 1996 Oct;67(4):1622-32
pubmed: 8858947
Front Cell Neurosci. 2014 Apr 23;8:113
pubmed: 24795568
J Neurosci Res. 2013 Jul;91(7):954-62
pubmed: 23606524
PLoS One. 2012;7(2):e31302
pubmed: 22312444
Neuron. 2009 Jan 15;61(1):85-100
pubmed: 19146815
Mol Neurodegener. 2017 Aug 15;12(1):59
pubmed: 28810892
Cell Mol Neurobiol. 2006 Oct-Nov;26(7-8):1085-97
pubmed: 16779670
FEBS Lett. 2012 Jan 2;586(1):47-54
pubmed: 22138183
Science. 1988 Jan 15;239(4837):285-8
pubmed: 3122323
Acta Neuropathol Commun. 2017 Dec 19;5(1):99
pubmed: 29258615
Curr Biol. 2010 Jun 8;20(11):1023-8
pubmed: 20471267
Mol Cell Neurosci. 2008 Apr;37(4):673-81
pubmed: 18272392
J Biol Chem. 2014 Oct 17;289(42):29322-33
pubmed: 25164813
Mol Neurodegener. 2007 Sep 06;2:17
pubmed: 17822548
Biochem J. 1990 Jul 1;269(1):61-4
pubmed: 2115775
J Neurosci. 2013 Jan 16;33(3):1024-37
pubmed: 23325240