Intracellular domains of amyloid precursor-like protein 2 interact with CP2 transcription factor in the nucleus and induce glycogen synthase kinase-3beta expression

Cell Death and Differentiation
Y XuY-H Suh

Abstract

Amyloid precursor protein (APP) is a member of a gene family that includes two APP-like proteins, APLP1 and 2. Recently, it has been reported that APLP1 and 2 undergo presenilin-dependent gamma-secretase cleavage, as does APP, resulting in the release of an approximately 6 kDa intracellular C-terminal domain (ICD), which can translocate into the nucleus. In this study, we demonstrate that the APLP2-ICDs interact with CP2/LSF/LBP1 (CP2) transcription factor in the nucleus and induce the expression of glycogen synthase kinase 3beta (GSK-3beta), which has broad-ranged substrates such as tau- and beta-catenin. The significance of this finding is substantiated by the in vivo evidence of the increase in the immunoreactivities for the nuclear C-terminal fragments of APLP2, and for GSK-3beta in the AD patients' brain. Taken together, these results suggest that APLP2-ICDs contribute to the AD pathogenesis, by inducing GSK-3beta expression through the interaction with CP2 transcription factor in the nucleus.

References

Nov 15, 1992·Proceedings of the National Academy of Sciences of the United States of America·W WascoF Solomon
Jan 1, 1991·Acta Neuropathologica·H Braak, E Braak
Apr 1, 1989·Trends in Neurosciences·R E TanziJ F Gusella
Apr 1, 1989·Proceedings of the National Academy of Sciences of the United States of America·D R RosenK White
Aug 1, 1995·Brain Research. Molecular Brain Research·T W KimI B Black
Dec 15, 1993·Proceedings of the National Academy of Sciences of the United States of America·I Daigle, C Li
Sep 28, 1999·Journal of Neuropathology and Experimental Neurology·J J PeiR F Cowburn
Sep 1, 2000·Brain Research. Brain Research Reviews·L BuéeP R Hof
Sep 20, 2000·Proceedings of the National Academy of Sciences of the United States of America·R V BhatC M Lee
Mar 29, 2001·Physiological Reviews·D J Selkoe
Apr 3, 2001·Journal of Medical Genetics·A E TaylorD C Rubinsztein
Aug 31, 2001·Progress in Neurobiology·C A Grimes, R S Jope
Mar 7, 2002·Trends in Molecular Medicine·Hagit Eldar-Finkelman
Jun 7, 2002·Current Opinion in Neurobiology·Michael D Kaytor, Harry T Orr
Aug 23, 2002·The Journal of Biological Chemistry·Shinji SatoAkihiko Takashima
Sep 14, 2002·The Journal of Biological Chemistry·Meir H ScheinfeldLuciano D'Adamio
Jun 26, 2003·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Ja Wook KooYoo-Hun Suh
Dec 31, 2003·The Journal of Biological Chemistry·Qiming Li, Thomas C Südhof
Apr 15, 2004·Molecular and Cellular Neurosciences·L PastorinoJ D Buxbaum
Feb 4, 2005·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Pei WangHui Zheng

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Citations

Mar 21, 2012·Molecular Neurodegeneration·Sonya B DumanisHyang-Sook Hoe
Nov 3, 2010·BMB Reports·Keun-A Chang, Yoo-Hun Suh
Aug 28, 2007·Neurochemistry International·Neville Marks, Martin J Berg
Sep 8, 2010·The Neuroscientist : a Review Journal Bringing Neurobiology, Neurology and Psychiatry·Ling Zhang
Oct 9, 2012·Macromolecular Bioscience·Rajesh Sunasee, Ravin Narain
Aug 17, 2018·BioMed Research International·Ankit TandonRajnish Kumar Chaturvedi
Nov 30, 2011·Journal of Neurochemistry·Raphaëlle Pardossi-Piquard, Frédéric Checler
Jul 4, 2017·Journal of Alzheimer's Disease : JAD·Craig MyrumTetyana Zayats
Nov 30, 2011·Journal of Neurochemistry·Han ZhangHuaxi Xu

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