control of axonal growth and regeneration of sensory neurons by the p110δ pi 3-kinase控制的感觉神经元的轴突生长和再生p110δπ3-kinase.pdf

Control of Axonal Growth and Regeneration of Sensory Neurons by the p110d PI 3-Kinase 1 1 2 3 3 2 3 Britta J. Eickholt *, Aminul I. Ahmed , Meirion Davies , Evangelia A. Papakonstanti , Wayne Pearce , Michelle L. Starkey , Antonio Bilancio , 4 5 2 6 4 2 3,7 Anna C. Need , Andrew J. H. Smith , Susan M. Hall , Frank P. Hamers , Karl P. Giese , Elizabeth J. Bradbury , Bart Vanhaesebroeck 1 Medical Research Council Centre for Developmental Neurobiology, King’s College London, London, United Kingdom, 2 Neurorestoration Group, Wolfson Centre for Age-Related Diseases, King’s College London, London, United Kingdom, 3 Ludwig Institute for Cancer Research, London, United Kingdom, 4 Centre for the Cellular Basis of Behaviour, Institute of Psychiatry, King’s College London, London, United Kingdom, 5 Gene Targeting Laboratory, The Institute for Stem Cell Research, University of Edinburgh, Edinburgh, United Kingdom, 6 Rudolf Magnus Institute of Neuroscience, University Medical Centre Utrecht, Utrecht, The Netherlands, 7 Department of Biochemistry and Molecular Biology, University College London, London, United Kingdom The expression and function of the 8 distinct catalytic isoforms of PI 3-kinase (PI3K) in the nervous system are unknown. Whereas most PI3Ks have a broad tissue distribution, the tyrosine kinase-linked p110d isoform has previously been shown to be enriched in leukocytes. Here we report that p110d is also highly expressed in the nervous system. Inactivation of p110d in mice did not affect gross neuronal d