ArticleThe Journal of biological chemistry2008
X11 proteins regulate the translocation of amyloid beta-protein precursor (APP) into detergent-resistant membrane and suppress the amyloidogenic cleavage of APP by beta-site-cleaving enzyme in brain.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 65 citations in OpenAlex.
- The AICD interactome: implications in neurodevelopment and neurodegeneration.Biochemical Society transactions · 2024Review
- Haploinsufficiency and Alzheimer's Disease: The Possible Pathogenic and Protective Genetic Factors.International journal of molecular sciences · 2024Review
- Suppression of the amyloidogenic metabolism of APP and the accumulation of Aβ by alcadein α in the brain during aging.Scientific reports · 2024Article
- Amyloid precursor protein and its interacting proteins in neurodevelopment.Biochemical Society transactions · 2023Review
- The US9-Derived Protein gPTB9TM Modulates APP Processing Without Targeting Secretase Activities.Molecular neurobiology · 2023Article
- Targeting the APP-Mint2 Protein-Protein Interaction with a Peptide-Based Inhibitor Reduces Amyloid-β Formation.Journal of the American Chemical Society · 2021Article
- Amyloidogenic processing of amyloid β protein precursor (APP) is enhanced in the brains of alcadein α-deficient mice.The Journal of biological chemistry · 2020Article
- Article
- Attenuation of amyloid-β generation by atypical protein kinase C-mediated phosphorylation of engulfment adaptor PTB domain containing 1 threonine 35.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- The physical approximation of APP and BACE-1: A key event in alzheimer's disease pathogenesis.Developmental neurobiology · 2018Review
- GULP1/CED-6 ameliorates amyloid-β toxicity in a Drosophila model of Alzheimer's disease.Oncotarget · 2017Article
- Association of Neuropathological Markers in the Parietal Cortex With Antemortem Cognitive Function in Persons With Mild Cognitive Impairment and Alzheimer Disease.Journal of neuropathology and experimental neurology · 2017Article
- APP Protein Family Signaling at the Synapse: Insights from Intracellular APP-Binding Proteins.Frontiers in molecular neuroscience · 2017Review
- Serotonin 6 receptor controls Alzheimer's disease and depression.Oncotarget · 2015Article
- Cytoplasmic fragment of Alcadein α generated by regulated intramembrane proteolysis enhances amyloid β-protein precursor (APP) transport into the late secretory pathway and facilitates APP cleavage.The Journal of biological chemistry · 2015Article
- Calmodulin Binding Proteins and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2015Article
- X11/Mint genes control polarized localization of axonal membrane proteins in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Hyperpolarization-activated cyclic nucleotide gated channels: a potential molecular link between epileptic seizures and Aβ generation in Alzheimer's disease.Molecular neurodegeneration · 2012Article
- Membrane-microdomain localization of amyloid β-precursor protein (APP) C-terminal fragments is regulated by phosphorylation of the cytoplasmic Thr668 residue.The Journal of biological chemistry · 2012Article
- The role of lipoprotein receptors on the physiological function of APP.Experimental brain research · 2012Review
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
X11 and X11-like proteins (X11L) are neuronal adaptor proteins whose association to the cytoplasmic domain of amyloid beta-protein precursor (APP) suppresses the generation of amyloid beta-protein (Abeta) implicated in Alzheimer disease pathogenesis. The amyloidogenic, but not amyloidolytic, metabolism of APP was selectively increased in the brain of mutant mice lacking X11L (Sano, Y., Syuzo-Takabatake, A., Nakaya, T., Saito, Y., Tomita, S., Itohara, S., and Suzuki, T. (2006) J. Biol. Chem. 281, 37853-37860). To reveal the actual role of X11 proteins (X11s) in suppressing amyloidogenic cleavage of APP in vivo, we generated X11 and X11L double knock-out mice and analyzed the metabolism of APP. The mutant mice showed enhanced beta-site cleavage of APP along with increased accumulation of Abeta in brain and increased colocalization of APP with beta-site APP-cleaving enzyme (BACE). In the brains of mice deficient in both X11 and X11L, the apparent relative subcellular distributions of both mature APP and its beta-C-terminal fragment were shifted toward the detergent-resistant membrane (DRM) fraction, an organelle in which BACE is active and both X11s are not nearly found. These results indicate that X11s associate primarily with APP molecules that are outside of DRM, that the dissociation of APP-X11/X11L complexes leads to entry of APP into DRM, and that cleavage of uncomplexed APP by BACE within DRM is enhanced by X11s deficiency. Present results lead to an idea that the dysfunction of X11L in the interaction with APP may recruit more APP into DRM and increase the generation of Abeta even if BACE activity did not increase in brain.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.