Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Electronic Gene Ontology annotations created by transferring manual GO annotations between related proteins based on shared sequence features
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Automatic assignment of GO terms using logical inference, based on on inter-ontology links
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
APP (horse, A0A3Q2IKB0): sequence and gene-model analysis
Horse A0A3Q2IKB0 versus human P05067 global alignment output
Horse APP UniProt/Ensembl gene-model comparison output
Experimental GO annotations of human, mouse and rat APP orthologs (QuickGO)
UniProt record for human APP (P05067)
PANTHER PTHR23103 family review
Amyloid precursor protein dimerization and synaptogenic function depend on copper binding to the growth factor-like domain.
Presynaptic and postsynaptic interaction of the amyloid precursor protein promotes peripheral and central synaptogenesis.
The beta-amyloid precursor protein of Alzheimer's disease enhances neuron viability and modulates neuronal polarity.
Production of amyloid beta protein precursor as a proteinase inhibitor by human astrocytic tumors.
A learning deficit related to age and beta-amyloid plaques in a mouse model of Alzheimer's disease.
Amyloid-beta induces chemotaxis and oxidant stress by acting at formylpeptide receptor 2, a G protein-coupled receptor expressed in phagocytes and brain.
Beta-amyloid activates the mitogen-activated protein kinase cascade via hippocampal alpha7 nicotinic acetylcholine receptors: In vitro and in vivo mechanisms related to Alzheimer's disease.
The amyloid precursor protein and its regulatory protein, FE65, in growth cones and synapses in vitro and in vivo.
RAGE potentiates Abeta-induced perturbation of neuronal function in transgenic mice.
Neuronal sorting protein-related receptor sorLA/LR11 regulates processing of the amyloid precursor protein.
ADAM19 is tightly associated with constitutive Alzheimer's disease APP alpha-secretase in A172 cells.
Biochemical and immunohistochemical analysis of an Alzheimer's disease mouse model reveals the presence of multiple cerebral Abeta assembly forms throughout life.
Memory impairment in transgenic Alzheimer mice requires cellular prion protein.
Activation of nicotinic α(7) acetylcholine receptor enhances long term potentation in wild type mice but not in APP(swe)/PS1ΔE9 mice.
TLR2 is a primary receptor for Alzheimer's amyloid β peptide to trigger neuroinflammatory activation.
A multimodal RAGE-specific inhibitor reduces amyloid β-mediated brain disorder in a mouse model of Alzheimer disease.
Amyloid β (Aβ) peptide directly activates amylin-3 receptor subtype by triggering multiple intracellular signaling pathways.
Antimicrobial activity of human islet amyloid polypeptides: an insight into amyloid peptides' connection with antimicrobial peptides.
Structural basis for endosomal trafficking of diverse transmembrane cargos by PX-FERM proteins.
FcγRIIb mediates amyloid-β neurotoxicity and memory impairment in Alzheimer's disease.
Activity-induced convergence of APP and BACE-1 in acidic microdomains via an endocytosis-dependent pathway.
Pharmacologic inhibition of ROCK2 suppresses amyloid-β production in an Alzheimer's disease mouse model.
High-resolution NMR characterization of low abundance oligomers of amyloid-β without purification.
Inflammatory microglia are glycolytic and iron retentive and typify the microglia in APP/PS1 mice.
TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function.
Role of phosphorylation of Alzheimer's amyloid precursor protein during neuronal differentiation.
CD74 interacts with APP and suppresses the production of Abeta.
miR-15b reduces amyloid-β accumulation in SH-SY5Y cell line through targetting NF-κB signaling and BACE1.
Implications of Oligomeric Amyloid-Beta (oAβ(42)) Signaling through α7β2-Nicotinic Acetylcholine Receptors (nAChRs) on Basal Forebrain Cholinergic Neuronal Intrinsic Excitability and Cognitive Decline.