TAILIEUCHUNG - Báo cáo khoa học: Reducing expression of NAD+ synthesizing enzyme NMNAT1 does not affect the rate of Wallerian degeneration

p63 is a member of the p53 tumour suppressor family that includes p73. Thep63gene encodes a protein comprising an N-terminal transactivation domain, a DNA binding domain and an oligomerization domain, but var-ies in the organization of the C-terminus as a result of complex alternative splicing. | IFEBS Journal Reducing expression of NAD synthesizing enzyme NMNAT1 does not affect the rate of Wallerian degeneration Laura Conforti1 2 3 Lucie Janeckova1 Diana Wagner2 Francesca Mazzola4 Lucia Cialabrini4 Michele Di Stefano4 Giuseppe Orsomando4 Giulio Magni4 Caterina Bendotti5 Neil Smyth6 and Michael Coleman1 2 1 The Babraham Institute Cambridge UK 2 Center for Molecular Medicine University of Cologne ZMMK Germany 3 Schoolof BiomedicalSciences University of Nottingham UK 4 Dipartimento di Patologia Molecolare e Terapie Innovative Universita Politecnica delle Marche Ancona Italy 5 Mario Negri PharmacologicalResearch Institute Milan Italy 6 Schoolof BiologicalSciences University of Southampton UK Keywords axon Cre-loxP knockout NAD P NMNAT Wallerian degeneration Correspondence L. Conforti School of Biomedical Sciences D37c University of Nottingham Medical School Queen s MedicalCentre Nottingham NG7 2UH UK Fax 44 0 115 8231476 Tel 44 0 115 8230142 E-mail Present address Schoolof BiomedicalSciences University of Nottingham Medical School Queen s Medical Centre Nottingham NG7 2UH UK Received 7 March 2011 revised 4 May 2011 accepted 23 May 2011 doi NAD synthesizing enzyme NMNAT1 constitutes most of the sequence of neuroprotective protein WldS which delays axon degeneration by 10-fold. NMNAT1 activity is necessary but not sufficient for WldS neuroprotection in mice and 70 amino acids at the N-terminus of WldS derived from poly-ubiquitination factor Ube4b enhance axon protection by NMNAT1. NMNAT1 activity can confer neuroprotection when redistributed outside the nucleus or when highly overexpressed in vitro and partially in Drosophila. However the role of endogenous NMNAT1 in normal axon maintenance and in Wallerian degeneration has not been elucidated yet. To address this question we disrupted the Nmnatl locus by gene targeting. Homozygous Nmnatl knockout mice do not survive to birth indicating that .

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