γ-Secretase Heterogeneity in the Aph1 Subunit: Relevance for Alzheimer’s Disease
暂无分享,去创建一个
R. D'Hooge | B. Hyman | B. de Strooper | J. Wiltfang | R. Sciot | O. Berezovska | M. Jucker | L. Serneels | L. Moons | K. Craessaerts | E. Karran | P. May | M. Schäfer | B. Sprangers | H. Esselmann | T. Dejaegere | K. Horré | S. Paul | Zhixiang Yang | J. Van Biervliet | Tine Van Houtvin | Katrien Horré | J. van Biervliet
[1] R. D'Hooge,et al. Deficiency of Aph1B/C-γ-secretase disturbs Nrg1 cleavage and sensorimotor gating that can be reversed with antipsychotic treatment , 2008, Proceedings of the National Academy of Sciences.
[2] D. Price,et al. Alteration of BACE1-dependent NRG1/ErbB4 signaling and schizophrenia-like phenotypes in BACE1-null mice , 2008, Proceedings of the National Academy of Sciences.
[3] Se Hoon Choi,et al. Moderate Reduction of γ-Secretase: Is There a Therapeutic Sweet Spot? , 2007, The Journal of Neuroscience.
[4] H. Wen,et al. Moderate Reduction of γ-Secretase Attenuates Amyloid Burden and Limits Mechanism-Based Liabilities , 2007, The Journal of Neuroscience.
[5] E. Kremmer,et al. Pathological activity of familial Alzheimer’s disease-associated mutant presenilin can be executed by six different γ-secretase complexes , 2007, Neurobiology of Disease.
[6] Simon T. Bate,et al. Non-cognitive behaviours in an APP/PS1 transgenic model of Alzheimer's disease , 2007, Behavioural Brain Research.
[7] D. Selkoe,et al. Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide , 2007, Nature Reviews Molecular Cell Biology.
[8] Hartwig Wolburg,et al. Aβ42‐driven cerebral amyloidosis in transgenic mice reveals early and robust pathology , 2006, EMBO reports.
[9] M. Gill,et al. Four Components Describe Behavioral Symptoms in 1,120 Individuals with Late‐Onset Alzheimer's Disease , 2006, Journal of the American Geriatrics Society.
[10] Angeliki Louvi,et al. Notch signalling in vertebrate neural development , 2006, Nature Reviews Neuroscience.
[11] S. Takeo,et al. Changes in the expression of Hes5 and Mash1 mRNA in the adult rat dentate gyrus after transient forebrain ischemia , 2005, Neuroscience Letters.
[12] B. Hyman,et al. Familial Alzheimer's Disease Presenilin 1 Mutations Cause Alterations in the Conformation of Presenilin and Interactions with Amyloid Precursor Protein , 2005, The Journal of Neuroscience.
[13] S. Hébert,et al. Differential contribution of the three Aph1 genes to γ-secretase activity in vivo , 2005 .
[14] D. Price,et al. APH-1a Is the Principal Mammalian APH-1 Isoform Present in γ-Secretase Complexes during Embryonic Development , 2005, The Journal of Neuroscience.
[15] S. Hébert,et al. Coordinated and widespread expression of γ-secretase in vivo: evidence for size and molecular heterogeneity , 2004, Neurobiology of Disease.
[16] C. Haass,et al. Identification of Distinct γ-Secretase Complexes with Different APH-1 Variants* , 2004, Journal of Biological Chemistry.
[17] B. de Strooper,et al. Partial loss of presenilins causes seborrheic keratosis and autoimmune disease in mice. , 2004, Human molecular genetics.
[18] Jay S. Fine,et al. Chronic Treatment with the γ-Secretase Inhibitor LY-411,575 Inhibits β-Amyloid Peptide Production and Alters Lymphopoiesis and Intestinal Cell Differentiation* , 2004, Journal of Biological Chemistry.
[19] B. Strooper,et al. Aph-1, Pen-2, and Nicastrin with Presenilin Generate an Active γ-Secretase Complex , 2003, Neuron.
[20] G. Arendash,et al. Behavioral characterization of the Tg2576 transgenic model of Alzheimer's disease through 19 months , 2002, Physiology & Behavior.
[21] Hugo Vanderstichele,et al. Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein , 1998, Nature.
[22] G. Schellenberg,et al. Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease , 1996, Nature Medicine.
[23] D. Borchelt,et al. Age-related CNS disorder and early death in transgenic FVB/N mice overexpressing Alzheimer amyloid precursor proteins , 1995, Neuron.