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APBB1 gene

Known as: APBB1, Fe65, AMYLOID BETA A4 PRECURSOR PROTEIN-BINDING, FAMILY B, MEMBER 1 
National Institutes of Health

Related topics

Related topics

2 relations
APBB1 protein, humanAPBB1IP gene

Papers overview

Semantic Scholar uses AI to extract papers important to this topic.
2012
2012
Degradation of mutant huntingtin via the ubiquitin/proteasome system is modulated by FE65.
An unstable expansion of the polyglutamine repeat within exon 1 of the protein Htt (huntingtin) causes HD (Huntington's disease… 
2012
2012
The Amyloid Precursor Protein Intracellular Domain-Fe65 Multiprotein Complexes: A Challenge to the Amyloid Hypothesis for Alzheimer's Disease?
Since its proposal in 1994, the amyloid cascade hypothesis has prevailed as the mainstream research subject on the molecular… 
Highly Cited
2007
Highly Cited
2007
RNA Interference Silencing of the Adaptor Molecules ShcC and Fe65 Differentially Affect Amyloid Precursor Protein Processing and Aβ Generation*
The amyloid precursor protein (APP) and its pathogenic by-product amyloid-β protein (Aβ) play central roles in Alzheimer disease… 
2007
2007
Axonal accumulation of synaptic markers in APP transgenic Drosophila depends on the NPTY motif and is paralleled by defects in synaptic plasticity
Alzheimer's disease (AD) is characterized by neurofibrillary tangles and extracellular plaques, which consist mainly of β‐amyloid… 
2007
2007
A macromolecular complex involving the amyloid precursor protein (APP) and the cytosolic adapter FE65 is a negative regulator of axon branching
2005
2005
Endoproteolytic Cleavage of FE65 Converts the Adaptor Protein to a Potent Suppressor of the sAPPα Pathway in Primates*
Adaptor protein FE65 (APBB1) specifically binds to the intracellular tail of the type I transmembrane protein, β-amyloid… 
2003
2003
Real-time PCR quantitation of FE65 a β-amyloid precursor protein-binding protein after traumatic brain injury in rats
In cases of traumatic brain injury (TBI) in which the patient survived for only a short period of time and was without… 
2002
2002
A candidate molecular mechanism for the association of an intronic polymorphism of FE65 with resistance to very late onset dementia of the Alzheimer type.
Late onset dementias of the Alzheimer type may be coupled to intrinsic aging processes. Their major pathological hallmarks are… 
Highly Cited
1999
Highly Cited
1999
A Single Point Mutation in a Group I WW Domain Shifts Its Specificity to That of Group II WW Domains*
WW domains can be divided into three groups based on their binding specificity. By random mutagenesis, we switched the… 
Highly Cited
1998
Highly Cited
1998
The human FE65 gene: genomic structure and an intronic biallelic polymorphism associated with sporadic dementia of the Alzheimer type
Abstract The FE65 protein binds to the intracellular domain of the beta-amyloid precursor protein (ßPP) and may modulate the… 
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