S. Soriano

发表

Presenilin Couples the Paired Phosphorylation of β-Catenin Independent of Axin Implications for β-Catenin Activation in Tumorigenesis

Edward H. Koo, B. Strooper, Hui Zheng, 2002, Cell.

Caspase cleavage of the amyloid precursor protein modulates amyloid β‐protein toxicity

D. Bredesen, E. Koo, S. Soriano, 2003, Journal of neurochemistry.

Expression of β-Amyloid Precursor Protein-CD3γ Chimeras to Demonstrate the Selective Generation of Amyloid β1–40and Amyloid β1–42 Peptides within Secretory and Endocytic Compartments*

Virginia M. Y. Lee, G. Stokin, X. Chen, 1999, The Journal of Biological Chemistry.

Mutagenesis Identifies New Signals for β-Amyloid Precursor Protein Endocytosis, Turnover, and the Generation of Secreted Fragments, Including Aβ42*

D. Selkoe, G. Stokin, W. Xia, 1999, The Journal of Biological Chemistry.

Loss of neuronal cell cycle control as a mechanism of neurodegeneration in the Presenilin-1 Alzheimer's disease brain

T. Hortobágyi, B. Malik, J. Cooper, 2008, Cell cycle.

Mutagenesis identifies new signals for beta-amyloid precursor protein endocytosis, turnover, and the generation of secreted fragments, including Abeta42.

D. Selkoe, G. Stokin, W. Xia, 1999, The Journal of biological chemistry.

Loss of amyloid precursor protein in a mouse model of Niemann–Pick type C disease exacerbates its phenotype and disrupts tau homeostasis

J. Cooper, S. Soriano, A. Nunes, 2011, Neurobiology of Disease.

Stability and bioactivity of chitosan as a transfection agent in primary human cell cultures: A case for chitosan-only controls.

W. Kirsch, S. Soriano, K. Oda, 2018, Carbohydrate polymers.

Loss of amyloid precursor protein exacerbates early inflammation in Niemann-Pick disease type C

Christopher G. Wilson, S. Soriano, D. Bellinger, 2019, Journal of Neuroinflammation.

The Nonconserved Hydrophilic Loop Domain of Presenilin (PS) Is Not Required for PS Endoproteolysis or Enhanced Aβ42 Production Mediated by Familial Early Onset Alzheimer's Disease-linked PS Variants*

T. Iwatsubo, E. Koo, M. Takahashi, 2000, The Journal of Biological Chemistry.

Filipin Levels as Potential Predictors of Alzheimer’s Disease Risk

S. Soriano, Michael A. Castello, Kristy Howard, 2014 .

Cell cycle‐driven neuronal apoptosis specifically linked to amyloid peptide Aβ1–42 exposure is not exacerbated in a mouse model of presenilin‐1 familial Alzheimer’s disease

B. Malik, S. Soriano, A. Currais, 2008, Journal of neurochemistry.

Caffeine Modulates Tau Phosphorylation and Affects Akt Signaling in Postmitotic Neurons

R. Ishii, L. Canuet, M. Takeda, 2011, Journal of Molecular Neuroscience.

A mutation in the calreticulin gene promoter in a family case of schizoaffective disorder leads to its aberrant transcriptional activation

H. Najmabadi, A. Aghajani, M. Ohadi, 2008, Brain Research.

The aspartate-257 of presenilin 1 is indispensable for mouse development and production of β-amyloid peptides through β-catenin-independent mechanisms

Hui Zheng, A. Takashima, H. Yamaguchi, 2002, Proceedings of the National Academy of Sciences of the United States of America.

Loss of presenilin 1 is associated with enhanced β-catenin signaling and skin tumorigenesis

Hui Zheng, E. Koo, S. Soriano, 2001, Proceedings of the National Academy of Sciences of the United States of America.

Presenilin 1 Negatively Regulates β-Catenin/T Cell Factor/Lymphoid Enhancer Factor-1 Signaling Independently of β-Amyloid Precursor Protein and Notch Processing

Hui Zheng, D. Kang, R. Pestell, 2001, The Journal of cell biology.

Presenilin 1 Facilitates the Constitutive Turnover of β-Catenin: Differential Activity of Alzheimer’s Disease–Linked PS1 Mutants in the β-Catenin–Signaling Pathway

M. Frosch, T. Collins, D. Kang, 1999, The Journal of Neuroscience.

Perturbed neurogenesis in the adult hippocampus associated with presenilin-1 A246E mutation.

E. Masliah, D. Kang, E. Koo, 2005, The American journal of pathology.

Presenilin couples the paired phosphorylation of beta-catenin independent of axin: implications for beta-catenin activation in tumorigenesis.

B. de Strooper, Hui Zheng, C. Eberhart, 2002, Cell.

Psychopathology and working memory‐induced activation of the prefrontal cortex in schizophrenia‐like psychosis of epilepsy: Evidence from magnetoencephalography

L. Canuet, M. Iwase, Hidetoshi Takahashi, 2011, Psychiatry and clinical neurosciences.

Moving beyond anti-amyloid therapy for the prevention and treatment of Alzheimer’s disease

S. Soriano, J. Jeppson, Michael A. Castello, 2014, BMC Neurology.

Short-term exposure to dietary cholesterol is associated with downregulation of interleukin-15, reduced thigmotaxis and memory impairment in mice

Christopher G. Wilson, S. Soriano, D. Bellinger, 2020, Behavioural Brain Research.

On the origin of Alzheimer's disease. Trials and tribulations of the amyloid hypothesis

S. Soriano, Michael A. Castello, 2014, Ageing Research Reviews.

Interaction between Oligomers of Stefin B and Amyloid-β in Vitro and in Cells*

V. Turk, V. Hodnik, G. Anderluh, 2009, The Journal of Biological Chemistry.

Cellular hormetic response to 27-hydroxycholesterol promotes neuroprotection through AICD induction of MAST4 abundance and kinase activity

Christopher G. Wilson, Traci L. Marin, H. Vinters, 2017, Scientific Reports.

Rational heterodoxy: Cholesterol reformation of the amyloid doctrine

S. Soriano, Michael A. Castello, 2013, Ageing Research Reviews.

The Amyloidogenic Pathway of Amyloid Precursor Protein (APP) Is Independent of Its Cleavage by Caspases*

S. Chandra, E. Koo, C. Pietrzik, 2001, The Journal of Biological Chemistry.

Cyclin-Dependent Kinase 5 Activator p25 Is Generated During Memory Formation and Is Reduced at an Early Stage in Alzheimer's Disease

T. Hortobágyi, C. Troakes, S. Al-Sarraj, 2011, Biological Psychiatry.

THE NEURONAL CELL CYCLE AS A MECHANISM OF PATHOGENESIS IN ALZHEIMER'S DISEASE

T. Hortobágyi, S. Soriano, A. Currais, 2008 .

Interferon downstream signaling is activated early in pre-symptomatic Niemann-Pick disease type C

Christopher G. Wilson, S. Soriano, D. Bellinger, 2019, Neuroscience Letters.

KIBRA Genetic Polymorphism Influences Episodic Memory in Alzheimer’s Disease, but Does Not Show Association with Disease in a Japanese Cohort

Takashi Morihara, Toshimitsu Hamasaki, Takashi Kudo, 2010, Dementia and Geriatric Cognitive Disorders.

The Notch intracellular domain represses CRE-dependent transcription.

S. Lovestone, K. Giese, M. Causevic, 2015, Cellular signalling.

Loss of amyloid precursor protein exacerbates early inflammation in Niemann-Pick disease type C

Christopher G. Wilson, S. Soriano, D. Bellinger, 2019, Journal of Neuroinflammation.

The aspartate-257 of presenilin 1 is indispensable for mouse development and production of beta-amyloid peptides through beta-catenin-independent mechanisms.

Hui Zheng, A. Takashima, H. Yamaguchi, 2002, Proceedings of the National Academy of Sciences of the United States of America.

PS1 Interacts With and Facilitates β-Catenin Turnover

D. Kang, E. Koo, S. Soriano, 2002 .

Cellular hormetic response to 27-hydroxycholesterol promotes neuroprotection through AICD induction of MAST4 abundance and kinase activity

Christopher G. Wilson, Traci L. Marin, H. Vinters, 2017, Scientific Reports.

The neuronal cell cycle as a mechanism of pathogenesis in Alzheimer's disease

T. Hortobágyi, S. Soriano, A. Currais, 2009, Aging.