Skip to search formSkip to main contentSkip to account menu

ADD3 wt Allele

Known as: ADDL, Adducin 3 (Gamma) wt Allele 
Human ADD3 wild-type allele is located within 10q24.2-q24.3 and is approximately 130 kb in length. This allele, which encodes gamma-adducin protein… 
National Institutes of Health

Related topics

Related topics

6 relations

Broader (1)

ADD3 gene
Cell MovementCytokinesisCytoskeletal ModelingMuscle Contraction

Papers overview

Semantic Scholar uses AI to extract papers important to this topic.
Review
2014
Review
2014
Targeting the proper amyloid-beta neuronal toxins: a path forward for Alzheimer’s disease immunotherapeutics
Levels of amyloid-beta monomer and deposited amyloid-beta in the Alzheimer’s disease brain are orders of magnitude greater than… 
Highly Cited
2011
Highly Cited
2011
Interaction between prion protein and toxic amyloid β assemblies can be therapeutically targeted at multiple sites
A role for PrP in the toxic effect of oligomeric forms of Aβ, implicated in Alzheimer's disease (AD), has been suggested but… 
Review
2011
Review
2011
Possible implications of insulin resistance and glucose metabolism in Alzheimer’s disease pathogenesis
•  Introduction •  Insulin, IGF‐1 in the brain •  Glucose metabolism and AD •  The insulin and IGF‐1 system in AD •  The insulin… 
Highly Cited
2010
Highly Cited
2010
Amyloid-β-Derived Diffusible Ligands Cause Impaired Axonal Transport of Mitochondria in Neurons
Background: Alzheimer’s disease (AD) is the most prevalent form of dementia predominantly affecting the elderly. It is believed… 
Review
2010
Review
2010
ADDLs and the signaling web that leads to Alzheimer’s disease
Highly Cited
2009
Highly Cited
2009
Inhibition of Calcineurin-mediated Endocytosis and α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid (AMPA) Receptors Prevents Amyloid β Oligomer-induced Synaptic Disruption
Synaptic degeneration, including impairment of synaptic plasticity and loss of synapses, is an important feature of Alzheimer… 
Highly Cited
2009
Highly Cited
2009
Insulin Receptor Dysfunction Impairs Cellular Clearance of Neurotoxic Oligomeric Aβ*
Accumulation of amyloid β (Aβ) oligomers in the brain is toxic to synapses and may play an important role in memory loss in… 
Highly Cited
2005
Highly Cited
2005
Transient overexpression of TGF-{beta}1 induces epithelial mesenchymal transition in the rodent peritoneum.
Epithelial mesenchymal transition (EMT), a process involved in many growth and repair functions, has been identified in the… 
Review
2002
Review
2002
Aβ toxicity in Alzheimer’s disease: globular oligomers (ADDLs) as new vaccine and drug targets
Highly Cited
1999
Highly Cited
1999
Assembly of Aβ Amyloid Protofibrils: An in Vitro Model for a Possible Early Event in Alzheimer's Disease†
Amyloid fibrils comprising primarily the peptides Aβ40 and Aβ42 are a defining feature of the Alzheimer's disease (AD) brain, and… 
By clicking accept or continuing to use the site, you agree to the terms outlined in our Privacy Policy (opens in a new tab), Terms of Service (opens in a new tab), and Dataset License (opens in a new tab)