Pages that link to "Q46663739"
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The following pages link to Disease-related modifications in tau affect the interaction between Fyn and Tau. (Q46663739):
Displaying 50 items.
- A phase Ib multiple ascending dose study of the safety, tolerability, and central nervous system availability of AZD0530 (saracatinib) in Alzheimer's disease (Q21146622) (← links)
- The novel cellular mechanism of human 5-HT6 receptor through an interaction with Fyn (Q24338247) (← links)
- Palmitoylation in Alzheimer's disease and other neurodegenerative diseases (Q26747019) (← links)
- Tau Oligomers: The Toxic Player at Synapses in Alzheimer's Disease (Q26773154) (← links)
- Alzheimer's Disease: Mechanism and Approach to Cell Therapy (Q26778149) (← links)
- Tangles, Toxicity, and Tau Secretion in AD - New Approaches to a Vexing Problem (Q27004724) (← links)
- Tau-targeted treatment strategies in Alzheimer's disease (Q27023429) (← links)
- Early etiology of Alzheimer's disease: tipping the balance toward autophagy or endosomal dysfunction? (Q27026907) (← links)
- Tau and tauopathies (Q27027415) (← links)
- Tau physiology and pathomechanisms in frontotemporal lobar degeneration (Q28070250) (← links)
- Tau Biology and Tau-Directed Therapies for Alzheimer's Disease (Q28071398) (← links)
- The Role of MAPT in Neurodegenerative Diseases: Genetics, Mechanisms and Therapy (Q28119005) (← links)
- Curcumin suppresses soluble tau dimers and corrects molecular chaperone, synaptic, and behavioral deficits in aged human tau transgenic mice (Q28282056) (← links)
- Critical residues involved in tau binding to fyn: implications for tau phosphorylation in Alzheimer's disease (Q30008912) (← links)
- Tau phosphorylation regulates the interaction between BIN1's SH3 domain and Tau's proline-rich domain (Q30009097) (← links)
- AlphaScreen HTS and live-cell bioluminescence resonance energy transfer (BRET) assays for identification of Tau-Fyn SH3 interaction inhibitors for Alzheimer disease (Q30009327) (← links)
- Interactions between the Fyn SH3-domain and adaptor protein Cbp/PAG derived ligands, effects on kinase activity and affinity. (Q30157613) (← links)
- Phosphorylation in the amino terminus of tau prevents inhibition of anterograde axonal transport. (Q30504709) (← links)
- Roles of tau protein in health and disease (Q33559303) (← links)
- Tau phosphorylation induced by severe closed head traumatic brain injury is linked to the cellular prion protein (Q33576693) (← links)
- Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. (Q33694502) (← links)
- Phosphorylation of tau at Y18, but not tau-fyn binding, is required for tau to modulate NMDA receptor-dependent excitotoxicity in primary neuronal culture (Q33709279) (← links)
- Mechanisms of tau-induced neurodegeneration (Q33859830) (← links)
- Tau potentiates nerve growth factor-induced mitogen-activated protein kinase signaling and neurite initiation without a requirement for microtubule binding. (Q33911246) (← links)
- Tyrosine phosphorylation of tau accompanies disease progression in transgenic mouse models of tauopathy. (Q34127161) (← links)
- Complex and Multidimensional Lipid Raft Alterations in a Murine Model of Alzheimer's Disease (Q34381556) (← links)
- Adaptors for disorders of the brain? The cancer signaling proteins NEDD9, CASS4, and PTK2B in Alzheimer's disease (Q34458459) (← links)
- Fyn inhibition rescues established memory and synapse loss in Alzheimer mice (Q34464152) (← links)
- The formation of tau pore-like structures is prevalent and cell specific: possible implications for the disease phenotypes (Q34506434) (← links)
- Oligomeric Aβ-induced synaptic dysfunction in Alzheimer's disease (Q34544243) (← links)
- Two motifs within the tau microtubule-binding domain mediate its association with the hsc70 molecular chaperone. (Q34743281) (← links)
- Tau in Alzheimer disease and related tauopathies (Q34953869) (← links)
- Alzheimer's disease neurofibrillary degeneration: pivotal and multifactorial (Q34974083) (← links)
- Dysregulation of protein phosphorylation/dephosphorylation in Alzheimer's disease: a therapeutic target (Q35016882) (← links)
- Roles of cholesterol and lipids in the etiopathogenesis of Alzheimer's disease (Q35016920) (← links)
- Profiling murine tau with 0N, 1N and 2N isoform-specific antibodies in brain and peripheral organs reveals distinct subcellular localization, with the 1N isoform being enriched in the nucleus (Q35081058) (← links)
- Developing pharmacological therapies for Alzheimer disease (Q35114786) (← links)
- Alzheimer neurofibrillary degeneration: significance, etiopathogenesis, therapeutics and prevention (Q35114797) (← links)
- The cellular distribution and Ser262 phosphorylation of tau protein are regulated by BDNF in vitro (Q35117516) (← links)
- Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation (Q35565682) (← links)
- Soluble Aβ oligomer production and toxicity (Q35663419) (← links)
- The many faces of tau (Q35870359) (← links)
- The protein phosphatase PP2A/Bα binds to the microtubule-associated proteins Tau and MAP2 at a motif also recognized by the kinase Fyn: implications for tauopathies. (Q35922428) (← links)
- Extracellular Tau levels are influenced by variability in Tau that is associated with tauopathies (Q36466732) (← links)
- Do axonal defects in tau and amyloid precursor protein transgenic animals model axonopathy in Alzheimer's disease? (Q36513243) (← links)
- Tau-Driven Neuronal and Neurotrophic Dysfunction in a Mouse Model of Early Tauopathy. (Q36587120) (← links)
- The complex PrP(c)-Fyn couples human oligomeric Aβ with pathological tau changes in Alzheimer's disease (Q36600160) (← links)
- Co-immunoprecipitation with Tau Isoform-specific Antibodies Reveals Distinct Protein Interactions and Highlights a Putative Role for 2N Tau in Disease (Q36778845) (← links)
- A decade of tau transgenic animal models and beyond (Q36817223) (← links)
- Diverse activation of microglia by chemokine (C-C motif) ligand 2 overexpression in brain (Q37053459) (← links)