We have analysed by northern blotting and by in situ hybridization the expression patterns of eight different genes during the second half of mouse embryonic development and in adult mouse brain: we compared the messenger RNA levels of amyloid precursor protein and of the two amyloid precursor protein-like proteins 1 and 2 and we have analysed expression of apolipoprotein E and of its main receptor in brain, the alpha-2-macroglobulin/low density lipoprotein receptor-related protein and three other ligands: the proteinase inhibitor alpha-2-macroglobulin, the modifying enzyme lipoprotein lipase and the 44,000 molecular weight heparin binding protein, a ligand of unknown function. During embryogenesis the temporal expression pattern differs considerably for the three members of the amyloid precursor proteins. Total embryo messenger RNA levels of amyloid precursor protein and amyloid precursor protein-like protein 2 increased progressively, while amyloid precursor protein-like protein 1 messenger RNA showed a burst of synthesis between days 10 and 13 post-coitum. Significantly, expression of the alpha-2-macroglobulin/low density lipoprotein receptor-related protein and of its associated protein, the 44,000 molecular weight heparin binding protein, exhibited their most important increase very similar to that of amyloid precursor protein-like protein 1, between days 10 and 13 post-coitum. Apolipoprotein E, lipoprotein lipase and alpha-2-macroglobulin messenger RNA levels in total embryos increased progressively, beginning most pronounced at days 13, 15 and 17, respectively. In mouse embryos, in situ hybridization established amyloid precursor protein, amyloid precursor protein-like protein 2 and alpha-2-macroglobulin/low density lipoprotein receptor-related protein messenger RNA to be expressed in most organs, with the notable exception of the liver, while expression of the other studied proteins was much more restricted. Among adult mouse tissues, the genes investigated were expressed very prominently in brain, except for lipoprotein lipase and for the complete absence of alpha-2-macroglobulin messenger RNA. In adult mouse brain, the cortex and hippocampus exhibited strong signals for most genes analysed. Exceptions are lipoprotein lipase and apolipoprotein E messenger RNAs, and the absent alpha-2-macroglobulin messenger RNA. Several interesting features, similarities as well as differences, between brain tissue sections hybridized with probes for amyloid precursor protein, amyloid precursor protein-like proteins 1 and 2 and between alpha-2-macroglobulin/low density lipoprotein receptor-related protein and heparin binding protein-44 were observed and are described. The results are further discussed in view of the known or anticipated physiological functions of the proteins examined and of their possible role in the etiology of Alzheimer's disease.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/0306-4522(94)00555-j | DOI Listing |
Nat Aging
January 2025
Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Korea.
The abnormal deposition of amyloid β (Aβ), produced by proteolytic cleavage events of amyloid precursor protein involving the protease γ-secretase and subsequent polymerization into amyloid plaques, plays a key role in the neuropathology of Alzheimer's disease (AD). Here we show that ErbB3 binding protein 1 (EBP1)/proliferation-associated 2G4 (PA2G4) interacts with presenilin, a catalytic subunit of γ-secretase, inhibiting Aβ production. Mice lacking forebrain Ebp1/Pa2g4 recapitulate the representative phenotypes of late-onset sporadic AD, displaying an age-dependent increase in Aβ deposition, amyloid plaques and cognitive dysfunction.
View Article and Find Full Text PDFExp Cell Res
January 2025
Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, 533000, China. Electronic address:
Background: Apurinic/apyrimidinic endodeoxyribonuclease 1 (APEX1) is involved in regulating the proliferation, invasion, migration, and other malignant progression of various cancer cells. However, its mechanism in clear cell renal cell carcinoma (ccRCC) remains unclear.
Methods: UALCAN database was performed to predict APEX1 expression in ccRCC.
Alzheimers Dement
January 2025
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Introduction: Plaques are a hallmark feature of Alzheimer's disease (AD). We found that the loss of mucosal-associated invariant T (MAIT) cells and their antigen-presenting molecule MR1 caused a delay in plaque pathology development in AD mouse models. However, it remains unknown how this axis is impacting dystrophic neurites.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Department of Neuroscience, Yale Medical School, New Haven, Connecticut, USA.
Aging rhesus macaques provide a unique model for learning how age and inflammation drive early-stage pathology in sporadic Alzheimer's disease, and for testing potential therapeutics. Unlike mice, aging macaques have extensive association cortices and inflammatory signaling similar to humans, are apolipoprotein E ε4 homozygotes, and naturally develop tau and amyloid pathology with marked cognitive deficits. Importantly, monkeys provide the unique opportunity to study early-stage, soluble hyperphosphorylated tau (p-tau), including p-tau217.
View Article and Find Full Text PDFMethods Mol Biol
January 2025
Department of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
This study describes an intramolecular quenching assay to evaluate gamma-secretase (GS) enzyme activity in human dermal cells. The method utilizes a fluorogenic peptide substrate, mimicking a fragment of amyloid precursor protein (APP), in which a quencher suppresses the fluorescence of a fluorophore until enzymatic cleavage occurs, resulting in a measurable increase in fluorescence. This real-time, direct measurement of GS activity allows for precise kinetic analysis using Michaelis-Menten modeling to define Kd and Vmax.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!