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Tytuł pozycji:

PI 3-kinase delta enhances axonal PIP 3 to support axon regeneration in the adult CNS.

Tytuł :
PI 3-kinase delta enhances axonal PIP 3 to support axon regeneration in the adult CNS.
Autorzy :
Nieuwenhuis B; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.; Laboratory for Regeneration of Sensorimotor Systems, Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences (KNAW), Amsterdam, The Netherlands.
Barber AC; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Evans RS; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Pearson CS; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Fuchs J; Institute of Biochemistry, Charité - Universitätsmedizin Berlin, Berlin, Germany.
MacQueen AR; Laboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge, UK.
van Erp S; MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
Haenzi B; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Hulshof LA; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Osborne A; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Conceicao R; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Khatib TZ; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Deshpande SS; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Cave J; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Ffrench-Constant C; MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK.
Smith PD; Department of Neuroscience, Carleton University, Ottawa, ON, Canada.
Okkenhaug K; Department of Pathology, University of Cambridge, Cambridge, UK.
Eickholt BJ; Institute of Biochemistry, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Martin KR; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.; Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, Melbourne, Vic., Australia.; Ophthalmology, Department of Surgery, University of Melbourne, Melbourne, Vic., Australia.
Fawcett JW; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.; Centre of Reconstructive Neuroscience, Institute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic.
Eva R; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
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Źródło :
EMBO molecular medicine [EMBO Mol Med] 2020 Aug 07; Vol. 12 (8), pp. e11674. Date of Electronic Publication: 2020 Jun 17.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
Język :
English
Imprint Name(s) :
Original Publication: Chichester, West Sussex : Wiley-Blackwell
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Grant Information :
BBS/E/B/000C0427 International UK Research and Innovation Biotechnology and Biological Sciences Research Council (BBSRC); CZ.02.1.01/0.0./0.0/15_003/0000419 International Czech Ministry of Education, Centre of Reconstructive Neuroscience; SFB TRR 186 International Deutsche Forschungsgemeinschaft (DFG); MR/R004544/1 United Kingdom MRC_ Medical Research Council; MR/R004544/1 International UK Research and Innovation, Medical Research Council (MRC); ALTF 1436-2015 International European Molecular Biology Organization (EMBO); 5065/5066 International Fight for Sight UK; TP10 International Deutsche Forschungsgemeinschaft (DFG); SFB 958 International Deutsche Forschungsgemeinschaft (DFG); MR/K017047/1 United Kingdom MRC_ Medical Research Council; International MRC Sackler; BBS/E/B/000C0409 United Kingdom BB_ Biotechnology and Biological Sciences Research Council; G0300336 United Kingdom MRC_ Medical Research Council; MR/R004463/1 United Kingdom MRC_ Medical Research Council; International Cambridge Eye Trust; International Christopher and Dana Reeve Foundation (Reeve Foundation); International ERA-NET Neuron grant AxonRepair; International Multiple Sclerosis Society (MS Society); 5119/5120 International Fight for Sight UK; MR/R004463/1 International UK Research and Innovation, Medical Research Council (MRC); 095691/Z/11/Z International Wellcome Trust (WT); International National Eye Research Centre (NERC); TP16 International Deutsche Forschungsgemeinschaft (DFG); NRB110 International International Spinal Research Trust
Contributed Indexing :
Keywords: CNS axon regeneration*; axon transport*; optic nerve*; p110 delta*; phosphoinositide 3-kinase*
Entry Date(s) :
Date Created: 20200620 Latest Revision: 20210317
Update Code :
20210318
PubMed Central ID :
PMC7411663
DOI :
10.15252/emmm.201911674
PMID :
32558386
Czasopismo naukowe
Peripheral nervous system (PNS) neurons support axon regeneration into adulthood, whereas central nervous system (CNS) neurons lose regenerative ability after development. To better understand this decline whilst aiming to improve regeneration, we focused on phosphoinositide 3-kinase (PI3K) and its product phosphatidylinositol (3,4,5)-trisphosphate (PIP 3 ). We demonstrate that adult PNS neurons utilise two catalytic subunits of PI3K for axon regeneration: p110α and p110δ. However, in the CNS, axonal PIP 3 decreases with development at the time when axon transport declines and regenerative competence is lost. Overexpressing p110α in CNS neurons had no effect; however, expression of p110δ restored axonal PIP 3 and increased regenerative axon transport. p110δ expression enhanced CNS regeneration in both rat and human neurons and in transgenic mice, functioning in the same way as the hyperactivating H1047R mutation of p110α. Furthermore, viral delivery of p110δ promoted robust regeneration after optic nerve injury. These findings establish a deficit of axonal PIP 3 as a key reason for intrinsic regeneration failure and demonstrate that native p110δ facilitates axon regeneration by functioning in a hyperactive fashion.
(© 2020 The Authors. Published under the terms of the CC BY 4.0 license.)

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