ArticleJournal of cellular and molecular medicine2008
C-terminal 37 residues of LRP promote the amyloidogenic processing of APP independent of FE65.
Article in Journal of cellular and molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Low-Density Lipoprotein Receptor-Related Protein 1 as a Potential Therapeutic Target in Alzheimer's Disease.Pharmaceutics · 2024Review
- Cholesterol-dependent amyloid β production: space for multifarious interactions between amyloid precursor protein, secretases, and cholesterol.Cell & bioscience · 2023Review
- COPS5 protein overexpression increases amyloid plaque burden, decreases spinophilin-immunoreactive puncta, and exacerbates learning and memory deficits in the mouse brain.The Journal of biological chemistry · 2015Article
- COPS5 (Jab1) protein increases β site processing of amyloid precursor protein and amyloid β peptide generation by stabilizing RanBP9 protein levels.The Journal of biological chemistry · 2013Article
- RanBP9 aggravates synaptic damage in the mouse brain and is inversely correlated to spinophilin levels in Alzheimer's brain synaptosomes.Cell death & disease · 2013Article
- Exploring the contribution of estrogen to amyloid-Beta regulation: a novel multifactorial computational modeling approach.Frontiers in pharmacology · 2013Article
- Low-density lipoprotein receptor-related protein 1: a physiological Aβ homeostatic mechanism with multiple therapeutic opportunities.Pharmacology & therapeutics · 2012Review
- Role of RanBP9 on amyloidogenic processing of APP and synaptic protein levels in the mouse brain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- A fragment of the scaffolding protein RanBP9 is increased in Alzheimer's disease brains and strongly potentiates amyloid-beta peptide generation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Proteolytic and non-proteolytic roles of membrane type-1 matrix metalloproteinase in malignancy.Biochimica et biophysica acta · 2010Review
- Novel role of RanBP9 in BACE1 processing of amyloid precursor protein and amyloid beta peptide generation.The Journal of biological chemistry · 2009Article
- TGF beta2-induced changes in LRP-1/T beta R-V and the impact on lysosomal A beta uptake and neurotoxicity.Brain research · 2008Article
- Structural studies of the transmembrane C-terminal domain of the amyloid precursor protein (APP): does APP function as a cholesterol sensor?Biochemistry · 2008Article
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Authors and funding
4 authors.
Funding
Abstract
The major defining pathological hallmark of Alzheimer's disease (AD) is the accumulation of amyloid beta protein (Abeta), a small peptide derived from beta- and gamma-secretase cleavages of the amyloid precursor protein (APP). Recent studies have shown that the Low-density lipoprotein receptor-related protein (LRP) plays a pivotal role in the trafficking of APP and generation of Abeta. In particular, we recently showed that the soluble cytoplasmic tail of LRP (LRP-ST) without a membrane tether was sufficient to promote Abeta generation. In this study, we demonstrate that the last 37 residues of LRP cytoplasmic tail (LRP-C37) lacking the NPxY motifs and FE65 binding mediate the core pro-amyloidogenic activity of LRP-ST. Moreover, we show that the conserved dileucine motif within the LRP-C37 region is a key determinant of its Abeta promoting activity. Finally, results from a yeast two-hybrid screen using LRP-C37 region as bait reveal four new LRP-binding proteins implicated in intracellular signalling and membrane protein trafficking. Our findings indicate that the LRP-C37 sequence represents a new protein-binding domain that may be useful as a therapeutic target and tool to lower Abeta generation in AD.
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