5 edition of Expression of human apolipoprotein E₄ in the central nervous system of transgenic mice found in the catalog.
|Series||Acta biomedica Lovaniensia ;, 210|
|LC Classifications||MLCM 2002/02365|
|The Physical Object|
|Pagination||v, 115 p. :|
|Number of Pages||115|
|LC Control Number||00333031|
Fryer JD, Demattos RB, McCormick LM, O’Dell MA, Spinner ML, Bales KR, Paul SM, Sullivan PM, Parsadanian M, Bu G, Holtzman DM () The low density lipoprotein receptor regulates the level of central nervous system human and murine apolipoprotein E but does not modify amyloid plaque pathology in PDAPP by: Abstract. An kilobase (kb) P1 bacteriophage clone (p) spanning the mouse apolipoprotein (apo) B gene was used to generate transgenic mice that express high levels of mouse levels of apoB, low density lipoprotein cholesterol, and low density lipoprotein triglycerides were increased, and high density lipoprotein cholesterol levels were decreased in the transgenic mice.
By generating PS tau transgenic mice on either a human ApoE knock-in (KI) or ApoE knockout (KO) background, here we show that PS/E4 mice have significantly higher tau levels in the brain and Cited by: Low density lipoprotein receptor-related protein mediates apolipoprotein E-dependent neurite outgrowth in a central nervous system-derived neuronal cell line. Proc. Natl Acad. Sci. Cited by:
Abstract. Apolipoprotein E (apoE) and apoE/amyloid-(A) transgenic (Tg) mouse models are critical to understanding apoE-isoform effects on Alzheimer's disease ed to wild type, mice exhibit neuronal deficits, similar to apoE4-Tg compared to apoE3-Tg mice, providing a model for A-independent apoE effects on determine the effects of apoE Cited by: Abstract. Apolipoprotein D (Apo D) and Apolipoprotein J (Apo J) are among the only nine apolipoproteins synthesized in the nervous system. Apart from development, these apolipoproteins are implicated in the normal aging process as well as in different neuropathologies as Alzheimer’s disease (AD), where a neuroprotective role has been : Eva del Valle, Ana Navarro, Eva Martínez-Pinilla, Silvia Torices, Jorge Tolivia.
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Expression of human apolipoprotein B and assembly of lipoprotein(a) in transgenic mice. Life Sciences Division, Lawrence Berkeley Laboratory, University of California, Berkeley Human apolipoprotein E2, E3, and E4 isoform-specific transgenic mice: human-like pattern of glial and neuronal immunoreactivity in central nervous system not observed in wild-type mice.
Xu PT(1), Schmechel D, Rothrock-Christian T, Burkhart DS, Qiu HL, Popko B, Sullivan P, Maeda N, Saunders AM, Roses AD, Gilbert by: To determine the effect of apoC-IV gene expression on lipoprotein metabolism, transgenic mice were generated using a human apoC-IV cDNA construct.
Human apoC-IV was found associated with plasma lipoproteins (d by: The impact of expression of human apolipoprotein E4 in different cell types in the brain was examined by generating transgenic mice expressing human ApoE4 in neurons or glial cells.
Mice transgenic for human ApoE4 expressed the transgene exclusively in neurons when under control of the Thy1 or PDGF gene promoters and in astrocytes when under control of Cited by: S.
() Expression of human apolipoprotein B90 in transgenic mice. Demonstration that apolipoprotein B90 lacks the structural requirements to form lipoprotein(a). Xianlin Han, Hua Cheng, John D. Fryer, Anne M. Fagan, David M. Holtzman. Expression of apoE in the central nervous system (CNS) in rodents is primarily in astrocytes, and is upregulated upon injury (18).
The role of apoE in the CNS is not well established. No neurological effects have been noted in human apoE-deficient subjects, and apoE-deficient mice have no developmental by: The human apoB transgenic mice were crossed with a previously described line of transgenic mice expressing human apo(a) cDNA 2.
The resulting combined transgenic animals expressing both human apoB and human apo(a) produced an Lp(a) particle sharing many properties with Lp(a) present in the plasma of : Edward M. Rubin. Apolipoprotein E (apoE) functions as an important carrier protein in the redistribution of lipids among cells (1).
The brain is second only to the liver with respect to apoE expression levels, and evidence has been accumulating rapidly that apoE plays a critical role in central nervous system (CNS) integrity, function, and repair after injury (2–5).Cited by: Here we show that transgenic mice expressing human apolipoprotein(a) are more susceptible than control mice to the development of lipid-staining lesions in the aorta, and that apolipoprotein(a).
Human apoE3 and apoE4 in brains and C SF of transgenic mice. A, Western blot analysis showing apoE expression in whole-brain homogenates (n 2 mice/genotype, 50 g protein / lane) and C SF (14 l. Expression of human apolipoprotein E4 in neurons causes hyperphosphorylation of protein tau in the brains of transgenic mice Epidemiological studies have established that the epsilon 4 allele of the ApoE gene (ApoE4) constitutes an important risk factor for Alzheimer's disease and might influence the outcome of central nervous system by: The apolipoprotein (Apo) AI-CIII-AIV gene cluster has a complex pattern of gene expression that is modulated by both gene- and cluster-specific cis-acting particular the regulation of Apo AIV expression has been previously studied in vivo and in vitro including several transgenic mouse lines but a complete, consistent picture of the tissue-specific Cited by: 9.
In the central nervous system, apoE is synthesized by glial cells and neurons, but it is unclear whether the cellular source affects its biological activities. To address this issue, we induced excitotoxic injury by systemic kainic acid injection in transgenic Apoe knockout mice expressing human apoE isoforms in astrocytes or neurons.
Regardless of its cellular source, apoE3 expression protected neuronal synapses and dendrites against the excitotoxicity seen in apoE-deficient Cited by: Apolipoprotein E (APOE) is a member of the lipoprotein family of cholesterol transporters.
Within the central nervous system (CNS), it mediates functions that are critical for neuronal development, plasticity, and repair [48,49].
The three most prevalent APOE isoforms are differentially encoded by the APOE ε2, ε3, and ε4 allele variants . Even more common are the problems of aging which are not due to disease but to more subtle impairments in neurobiological systems, including impairments in vision, memory loss, muscle weakening, and loss of reproductive functions, changes in body weight, and sleeplessness.
Transgenic mice (Tg) overexpressing human apolipoprotein D (H-apoD) in the brain are resistant to neurodegeneration. Despite the use of a neuron-specific promoter to generate the Tg. The rats were produced by microinjection of a 13 kbp DNA fragment containing the human apolipoprotein A-I gene plus 10 kbp of its 5′ flanking sequence and 1 kbp of its 3′ flanking sequence.
Both lines of transgenic rats express human apolipoprotein A-I mRNA in liver and human apolipoprotein A-I in by: Model of Genetic Susceptibility to Late-Onset Alzheimer’s Disease: Mice Transgenic for Human Apolipoprotein E Alleles A. D.,Neurodegenera-tion in the central nervous system of apoE-deficient mice, Exp.
Neurol. – control region directs expression of the linked human apolipoprotein E and C1 genes in transgenic mice, J Cited by: 1. Abstract. Type III hyperlipoproteinemia (HLP) is a genetic disorder of lipid metabolism in humans in which the primary molecular defect is a mutation(s) in apolipoprotein (apo) E that causes defective interaction of apoE with lipoprotein receptors and an accumulation of cholesterol-rich β-VLDL in the blood (Mahley and Rall, ).Author: Stanley C.
Rall, Yukio Horie, Sergio Fazio. Increased atherosclerosis and vascular inflammation in APP transgenic mice with apolipoprotein E deficiency Article in Atherosclerosis (1) May with 24 Reads How we measure 'reads'.Introduction. Human apolipoprotein E (ApoE) is located on chromosome 19 and encodes a 35 kDa glycoprotein  that exists in three isoforms: E2, E3 and E4 [2,3].These isoforms differ by amino acid substitutions at two positions (residues and ) .The amino acid changes are believed to alter the protein charge and stability , thereby contributing to its distinctive.
Human IgH loci. a The complete V H, D and J H region from the most 5′ V H, IgHV3–74, to the most 3′ J H segment, J H 6, is accommodated on ~ kb (Lefranc and Lefranc ). b Transgenic constructs and features. Animals were derived from manipulated fibroblasts (cattle) or ES cells (mouse) and by DNA microinjection (mouse and rat).
In several lines, human Ig expression Cited by: