Area of research
Physiology · Molecular Biology
Research interest
Research focused on Hyperphosphorylation and Phosphorylation, with related work in Tau protein, Tauopathy, Tau pathology. Notable publications include 'Cross talk between PI3K-AKT-GSK-3β and PP2A pathways determines tau hyperphosphorylation', 'Hyperphosphorylation determines both the spread and the morphology of tau pathology', and 'Pathological Tau From Alzheimer’s Brain Induces Site-Specific Hyperphosphorylation and SDS- and Reducing Agent-Resistant Aggregation of Tau in vivo'.
Rhythmic TDP-43 affects RNA splicing of USP13, resulting in alteration of BMAL1 ubiquitination
Dual-specificity tyrosine phosphorylation-regulated kinase 1A promotes the inclusion of amyloid precursor protein exon 7
Tau truncation in the pathogenesis of Alzheimer’s disease: a narrative review
C9orf72 <scp>poly‐PR</scp> helps p53 escape from the ubiquitin‐proteasome system and promotes its stability
Passive immunization inhibits tau phosphorylation and improves recognition learning and memory in 3xTg-AD mice
c-Src regulates δ-secretase activation and truncated Tau production by phosphorylating the E3 ligase Traf6
SIRT1 deficiency increases O-GlcNAcylation of tau, mediating synaptic tauopathy
Tau antibody <scp>77G7</scp> targeting microtubule binding domain suppresses proteopathic tau to seed tau aggregation
Tau seeding activity in various regions of down syndrome brain assessed by two novel assays
A novel dephosphorylation targeting chimera selectively promoting tau removal in tauopathies
Phosphorylation of trans‐active response DNA‐binding protein‐of 43 kDa promotes its cytoplasmic aggregation and modulates its function in tau mRNA stability and exon 10 alternative splicing
Excess Folic Acid Supplementation before and during Pregnancy and Lactation Alters Behaviors and Brain Gene Expression in Female Mouse Offspring
Dephosphorylation Passivates the Seeding Activity of Oligomeric Tau Derived From Alzheimer’s Brain
Truncation of Tau selectively facilitates its pathological activities
Tau in Alzheimer’s Disease: Pathological Alterations and an Attractive Therapeutic Target
SIRT1 regulates O-GlcNAcylation of tau through OGT
Expression of Microtubule Associated Protein Tau in Mouse Pancreatic Islets Is Restricted to Autonomic Nerve Fibers
Effect of Peripheral Insulin Administration on Phosphorylation of Tau in the Brain
Pathological Tau From Alzheimer’s Brain Induces Site-Specific Hyperphosphorylation and SDS- and Reducing Agent-Resistant Aggregation of Tau in vivo
Pathological Alterations of Tau in Alzheimer’s Disease and 3xTg-AD Mouse Brains
Excess Folic Acid Supplementation Before and During Pregnancy and Lactation Activates Fos Gene Expression and Alters Behaviors in Male Mouse Offspring
Intranasal Administration of Insulin Reduces Chronic Behavioral Abnormality and Neuronal Apoptosis Induced by General Anesthesia in Neonatal Mice
Elevation of casein kinase 1ε associated with TDP‐43 and tau pathologies in Alzheimer's disease
Subacute to chronic Alzheimer-like alterations after controlled cortical impact in human tau transgenic mice
Relevance of Phosphorylation and Truncation of Tau to the Etiopathogenesis of Alzheimer’s Disease
Pathological Changes of Tau Related to Alzheimer’s Disease
Mechanism of Tau Hyperphosphorylation Involving Lysosomal Enzyme Asparagine Endopeptidase in a Mouse Model of Brain Ischemia
Neuronal O-GlcNAc transferase regulates appetite, body weight, and peripheral insulin resistance
Involvement of Activation of Asparaginyl Endopeptidase in Tau Hyperphosphorylation in Repetitive Mild Traumatic Brain Injury
Dyrk1A overexpression leads to increase of 3R-tau expression and cognitive deficits in Ts65Dn Down syndrome mice