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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 30 May 2015.

Amyloid beta

APP, Abeta
This gene encodes a cell surface receptor and transmembrane precursor protein that is cleaved by secretases to form a number of peptides. Some of these peptides are secreted and can bind to the acetyltransferase complex APBB1/TIP60 to promote transcriptional activation, while others form the protein basis of the amyloid plaques found in the brains of patients with Alzheimer disease. Mutations in this gene have been implicated in autosomal dominant Alzheimer disease and cerebroarterial amyloidosis (cerebral amyloid angiopathy). Multiple transcript variants encoding several different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Presenilin-1, CAN, AGE, beta-secretase, V1a
Papers using APP antibodies
The anti-cholinesterase phenserine and its enantiomer Posiphen as 5′ untranslated region directed translation blockers of the Parkinson's alpha synuclein expression
Greig Nigel H et al., In Journal of Neurology, Neurosurgery, and Psychiatry, 2011
... Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of ...
TrkB and protein kinase Mzeta regulate synaptic localization of PSD-95 in developing cortex
Rivest Serge et al., In Frontiers in Cellular Neuroscience, 2010
... (B6.129S4-Ccr2tm1Ifc/J) and APP transgenic mice (APP ...
The projected effect of risk factor reduction on Alzheimer's disease prevalence.
Ginsberg Stephen D., In PLoS ONE, 2010
... Rabbit polyclonal antibody against amyloid precursor protein (APP) was from Novus Biologicals (Littleton, CO) ...
Neurogenesis and Alzheimer's disease: At the crossroads.
Gaetani Silvana, In PLoS ONE, 2008
... For all experiments, we used age-matched littermate female mice obtained from heterozygous APPSw,Ind x non-transgenic (WT) crossings ...
Beta-secretase-1 elevation in transgenic mouse models of Alzheimer’s disease is associated with synaptic/axonal pathology and amyloidogenesis: implications for neuritic plaque development
Gutierrez Antonia et al., In Acta Neuropathologica, 2008
... The generation and characterization of PS1/APP transgenic (tg) mice has been ...
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Papers on APP
Familial late-onset Alzheimer's disease: description of an Italian family with four affected siblings and one case of early-onset dementia in the preceding generation.
Mari et al., Milano, Italy. In Aging Clin Exp Res, 27 Jun 2015
We constructed the family pedigree, evaluated mutations usually associated with early-onset Alzheimer's disease (APP, PSEN1, PSEN2), and assessed polymorphisms in the apolipoprotein E (APOE) gene and in cytokine genes that we had previously found to be associated with a higher risk of LOAD (IL-10, IL-6, TNF-α).
Prion-Protein-Interacting Amyloid-β Oligomers of High Molecular Weight are Tightly Correlated with Memory Impairment in Multiple Alzheimer Mouse Models.
Strittmatter et al., United States. In J Biol Chem, 27 Jun 2015
Deleting PrP(C) expression in mice with relatively low PrP(C)-interacting Aβo (Tg2576) results in partial rescue of cognitive performance as opposed to complete recovery in animals with a high percentage of PrP(C)-interacting Aβo (APP/PSEN1).
Laminar Specific Detection of APP induced Neurodegeneration and Recovery using MEMRI in an Olfactory based Alzheimer's Disease Mouse Model.
Koretsky et al., Bethesda, United States. In Neuroimage, 25 Jun 2015
UNASSIGNED: Manganese Enhanced MRI (MEMRI) was used to detect specific laminar changes in the olfactory bulb (OB) to follow the progression of amyloid precursor protein (APP)-induced neuronal pathology and its recovery in a reversible olfactory based Alzheimer's disease (AD) mouse model.
Diffuse Axonal Injury-A Distinct Clinicopathological Entity in Closed Head Injuries.
Balazic et al., Скопје, Macedonia. In Am J Forensic Med Pathol, 22 Jun 2015
In terms of its biomechanics, DAI is occurring as a result of acceleration forces of longer duration and has been fully reproduced experimentally.In the process of diagnosing DAI, the performance of a complete forensic neuropathological examination is essential and the immunohistochemistry method using antibodies against β-amyloid precursor protein (β-APP) has been proved to be highly sensitive and specific, selectively targeting the damaged axons.In this review, we are pointing to the significant characteristics of DAI as a distinct clinicopathological entity that can cause severe impairment of the brain function, and in the forensic medicine setting, it can be found as the concrete cause of death.
Elucidating molecular phenotypes caused by the SORL1 Alzheimer's disease genetic risk factor using human induced pluripotent stem cells.
Goldstein et al., San Diego, United States. In Cell Stem Cell, 02 May 2015
We found that human neurons carrying SORL1 variants associated with an increased SAD risk show a reduced response to treatment with BDNF, at the level of both SORL1 expression and APP processing.
Body fluid biomarkers in Alzheimer's disease.
Tan et al., Nanjing, China. In Ann Transl Med, 30 Apr 2015
We also review data from several novel biomarkers, such as, β-site APP cleaving enzyme 1, soluble amyloid precursor proteins α and β, soluble Aβ oligomers and so on, which are associated with the occurrence and deterioration of this disease and couldn't be ignored.
Longitudinal PET-MRI reveals β-amyloid deposition and rCBF dynamics and connects vascular amyloidosis to quantitative loss of perfusion.
Pichler et al., Tübingen, Germany. In Nat Med, Dec 2014
We present longitudinal in vivo data on the dynamics of β-amyloid deposition and the decline of rCBF in two different amyloid precursor protein (APP) transgenic mouse models of AD.
Additional mechanisms conferring genetic susceptibility to Alzheimer's disease.
Medina et al., Madrid, Spain. In Front Cell Neurosci, Dec 2014
Familial Alzheimer's disease (AD), mostly associated with early onset, is caused by mutations in three genes (APP, PSEN1, and PSEN2) involved in the production of the amyloid β peptide.
Activation of mTOR: a culprit of Alzheimer's disease?
Yan et al., Shiyan, China. In Neuropsychiatr Dis Treat, Dec 2014
More highlights demonstrate that the activation of the mammalian target of rapamycin (mTOR) enhances Aβ generation and deposition by modulating amyloid precursor protein (APP) metabolism and upregulating β- and γ-secretases.
Adapting for endocytosis: roles for endocytic sorting adaptors in directing neural development.
Winckler et al., Charlottesville, United States. In Front Cell Neurosci, Dec 2014
We focus our discussion on endocytic accessory proteins (EAPs) (such as numb and disabled) and how they regulate endocytosis and subsequent post-endocytic trafficking of their cognate receptors (such as Notch, TrkB, β-APP, VLDLR, and ApoER2).
Role of P2X7 and P2Y2 receptors on α-secretase-dependent APP processing: Control of amyloid plaques formation "in vivo" by P2X7 receptor.
Gualix et al., Madrid, Spain. In Comput Struct Biotechnol J, Dec 2014
Amyloid precursor protein (APP) is expressed in a large variety of neural and non-neural cells.
1950 MHz Electromagnetic Fields Ameliorate Aβ Pathology in Alzheimer's Disease Mice.
Lee et al., Seoul, South Korea. In Curr Alzheimer Res, Dec 2014
Notably, chronic RFEMF exposure significantly reduced not only Aβ plaques, APP, and APP carboxyl-terminal fragments (CTFs) in whole brain including hippocampus and entorhinal cortex but also the ratio of Aβ42 and Aβ40 peptide in the hippocampus of Tg-5xFAD mice.
Metastasis-suppressor transcript destabilization through TARBP2 binding of mRNA hairpins.
Tavazoie et al., New York City, United States. In Nature, Oct 2014
Endogenous TARBP2 promotes metastatic cell invasion and colonization by destabilizing amyloid precursor protein (APP) and ZNF395 transcripts, two genes previously associated with Alzheimer's and Huntington's disease, respectively.
The ongoing search for small molecules to study metal-associated amyloid-β species in Alzheimer's disease.
Lim et al., Ann Arbor, United States. In Acc Chem Res, Sep 2014
Amyloid-β (Aβ), generated from proteolytic processing of the amyloid precursor protein (APP), and its aggregated forms, particularly oligomers, are suggested as key pathological features in AD-affected brains.
Three-dimensional structure of human γ-secretase.
Shi et al., Beijing, China. In Nature, Sep 2014
Aberrant cleavage of the amyloid precursor protein (APP) results in aggregation of amyloid-β, which accumulates in the brain and consequently causes Alzheimer's disease.
Structural origin of polymorphism of Alzheimer's amyloid β-fibrils.
Guo et al., Los Angeles, United States. In Biochem J, 2012
propose that the strength of inter-strand side-chain interactions determines the degree of beta-sheet twist, which then leads to the different association patterns between different cross beta-units and thus distinct fibril morphologies
Down's syndrome and Alzheimer's disease: towards secondary prevention.
Manji et al., Trenton, United States. In Nat Rev Drug Discov, 2012
[review] Based on the apparent common pathogenic role of amyloid precursor protein in both Down's syndrome and Alzheimer's disease (AD), the idea that the dementia associated with Down's syndrome is in fact AD is supported on many levels.
Ubiquilin-1 regulates amyloid precursor protein maturation and degradation by stimulating K63-linked polyubiquitination of lysine 688.
Boehning et al., Galveston, United States. In Proc Natl Acad Sci U S A, 2012
These results reveal the mechanistic basis by which ubiquilin-1 regulates APP maturation.
Molecular basis of β-amyloid oligomer recognition with a conformational antibody fragment.
Fändrich et al., Halle, Germany. In Proc Natl Acad Sci U S A, 2012
Molecular basis of beta-amyloid oligomer recognition with a conformational antibody fragment.
Neurologic and motor dysfunctions in APP transgenic mice.
Strazielle et al., Mont-Saint-Aignan, France. In Rev Neurosci, 2011
In APP transgenic mice models showed Neurologic and motor dysfunctions.
More papers using APP antibodies
Rab8 is involved in zymogen granule formation in pancreatic acinar AR42J cells
da Cruz e Silva Odete AB et al., In Molecular Neurodegeneration, 2007
... Primary monoclonal antibodies used were 22C11 (Chemicon) against the APP ectodomain, JL-8 (BD Biosciences) for detection of the ...
Clinical study on a randomized, double-blind control of Shenwu gelatin capsule in treatment of mild cognitive impairment
Liu Jian-xun et al., In Evidence-based Complementary and Alternative Medicine : eCAM, 2006
... = 10), controlled for age (5 months, range 4–6), were separated into 4 groups: APP/PS1+tap water (transgenic group), ...
Immune effects of cocoa procyanidin oligomers on peripheral blood mononuclear cells
Jutila Mark A. et al., In Genes and immunity, 2006
... For transcript stabilization studies, cells in X-VIVO were treated with APP (Apple PolyR, Littleton, CO, USA) at 54μg/mL, recombinant human TNFα (PeproTech, Rocky Hill, NJ, USA) at 50ng/mL, recombinant bovine TNFα (Thermo Scientific, Waltham, MA), PC1 (Phytolab, ...
Role of APP phosphorylation in FE65-dependent gene transactivation mediated by AICD
Suzuki Toshiharu et al., In Molecular Neurodegeneration, 2005
... The APP-ibl transgenic mouse was generated ...
Deletion of tumor necrosis factor death receptor inhibits amyloid β generation and prevents learning and memory deficits in Alzheimer's mice
Shen Yong et al., In The Journal of Cell Biology, 2004
... Generation of APP transgenic AD mice with deletion ...
Functionalization and peptide-based delivery of magnetic nanoparticles as an intracellular MRI contrast agent
Li Feng et al., In Molecular therapy. Nucleic acids, 2003
... polyvinylidene fluoride membranes were incubated with antibody (BACE1 polyclonal antibody (1:1,000): AB5940; Millipore (Billerica, MA); APP monoclonal antibody (1:2,000): catalog number 1565-1; Epitomics (Burlingame, CA); β-actin monoclonal ...
Antibodies against beta-amyloid slow cognitive decline in Alzheimer's disease
Morgan Dave et al., In Journal of Neuroinflammation, 2002
... For the 5-month treatment study, 13 APP-transgenic mice, aged 23 months, ...
Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis
Grutzendler Jaime et al., In Scientific Reports, 2002
... Imaging Abeta plaques in living transgenic mice with multiphoton microscopy ...
Inhibition of huntingtin fibrillogenesis by specific antibodies and small molecules: implications for Huntington's disease therapy
Chang N-S et al., In Cell Death & Disease, 1999
... Antibody against phospho-APP at Thr668 was from Cell Signaling Technology (Danvers, MA, USA) ...
Sunday Driver links axonal transport to damage signaling
Goldstein Lawrence S.B. et al., In The Journal of Cell Biology, 1998
... Brady, University of Illinois, Chicago, IL), anti-DIC and anti-APP (Chemicon), anti-syntaxin13 (Synaptic Systems GmbH), anti-myelin basic protein ...
A simple statistical parameter for use in evaluation and validation of high throughput screening assays
Liebman Susan W. et al., In Disease Models & Mechanisms, 1998
... Correlative memory deficits, Abeta elevation, and amyloid plaques in transgenic mice ...
Coordinated transport of phosphorylated amyloid-β precursor protein and c-Jun NH2-terminal kinase–interacting protein-1
Muresan Virgil et al., In The Journal of Cell Biology, 1998
... 22C11; CHEMICON International, Inc.); mouse anti–human amyloid-β protein (clones 4G8 and 6E10; Signet Laboratories); rabbit anti-APP (raised against a polypeptide from the cytoplasmic domain of APP; Cell Signaling Technology); mouse anti–human APP ...
New software toolkits for comprehensive visualization and analysis of three-dimensional multimodal biomedical images.
Finkelstein David I., In PLoS ONE, 1996
... The APP mice were heterozygous transgenic mice (C57B6/SJL, I.D ...
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