gopubmed logo
 
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 30 Jun 2015.

Apolipoprotein Ea

apolipoprotein E
Top mentioned proteins: apolipoprotein E, AGE, HAD, CAN, V1a
Papers on apolipoprotein E
Flow-dependent expression of ectonucleotide tri(di)phosphohydrolase-1 and suppression of atherosclerosis.
New
Pinsky et al., In J Clin Invest, 29 Jul 2015
Here, we evaluated the contribution of CD39 to atherogenesis in the apolipoprotein E-deficient (ApoE-deficient) mouse model of atherosclerosis.
Targeting HSP90 ameliorates nephropathy and atherosclerosis through suppression of NF-κB and STAT signaling pathways in diabetic mice.
New
Gomez-Guerrero et al., Madrid, Spain. In Diabetes, 26 Jul 2015
Therefore, we investigated whether pharmacological HSP90 inhibition ameliorates diabetes-associated renal damage and atheroprogression in a mouse model of combined hyperglycemia and hyperlipidemia (streptozotocin-induced diabetic apolipoprotein E-deficient mouse).
The intravenous injection of oxidized LDL- or Apolipoprotein B100 - coupled splenocytes promotes Th1 polarization in wildtype and Apolipoprotein E - deficient mice.
New
Mallat et al., Paris, France. In Biochem Biophys Res Commun, 24 Jul 2015
In Apolipoprotein E - deficient (ApoE-/-) mice that received oxLDL-SP every 5 weeks for 20 weeks, we did not find any difference of atherosclerotic plaque burden, but again increased IFNγ production.
Zinc affects the proteolytic stability of Apolipoprotein E in an isoform-dependent way.
New
Adlard et al., Melbourne, Australia. In Neurobiol Dis, 24 Jul 2015
In this study we examined the effects of zinc on the proteolysis of synthetic Apolipoprotein E (ApoE), a protein whose allelic variants differentially contribute to the onset/progression of disease.
Interleukin 18 function in atherosclerosis is mediated by the interleukin 18 receptor and the Na-Cl co-transporter.
New
Impact
Shi et al., Boston, United States. In Nat Med, 22 Jul 2015
Here, we show that absence of the IL18 receptor (IL18r) does not affect atherosclerosis in apolipoprotein E-deficient (Apoe(-/-)) mice, nor does it affect IL18 cell surface binding to or signaling in endothelial cells.
Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis.
New
Impact
Zetterberg et al., Maastricht, Netherlands. In Jama, 19 Jun 2015
MAIN OUTCOMES AND MEASURES: Prevalence of amyloid pathology on positron emission tomography or in cerebrospinal fluid according to AD risk factors (age, apolipoprotein E [APOE] genotype, sex, and education) estimated by generalized estimating equations.
Prevalence of amyloid PET positivity in dementia syndromes: a meta-analysis.
New
Impact
Brooks et al., Maastricht, Netherlands. In Jama, 19 Jun 2015
MAIN OUTCOMES AND MEASURES: Estimated prevalence of positive amyloid PET scans according to diagnosis, age, and apolipoprotein E (APOE) ε4 status, using the generalized estimating equations method.
Association between apolipoprotein E gene polymorphism and depression.
Review
New
Sun et al., Hefei, China. In J Clin Neurosci, 12 Jun 2015
UNASSIGNED: We performed an updated meta-analysis to obtain a more precise estimation of the relationship between apolipoprotein E (ApoE) gene polymorphism and susceptibility to depression, as previous reports have been inconsistent.
Additional mechanisms conferring genetic susceptibility to Alzheimer's disease.
Review
New
Medina et al., Madrid, Spain. In Front Cell Neurosci, Dec 2014
Besides apolipoprotein E, that presents a strong association with the disease (OR∼4), the rest of these genes have moderate or low degrees of association, with OR ranging from 0.88 to 1.23.
The role of APOE-ɛ4 and beta amyloid in the differential rate of recovery from ECT: a review.
Review
New
Martins et al., Australia. In Transl Psychiatry, Dec 2014
A narrative review of the research literature on carriage of the apolipoprotein E ɛ4 allele (APOE-ɛ4) and the protein biomarker beta amyloid (Aβ) with ECT cognitive outcome was undertaken.
Link between type 2 diabetes and Alzheimer's disease: from epidemiology to mechanism and treatment.
Review
New
Leng et al., Dalian, China. In Clin Interv Aging, Dec 2014
It is worth mentioning that the therapeutic effects of these drugs are influenced by the apolipoprotein E (APOE)-ε4 genotype.
Comparing recruitment, retention, and safety reporting among geographic regions in multinational Alzheimer's disease clinical trials.
New
Cummings et al., Irvine, United States. In Alzheimers Res Ther, Dec 2014
RESULTS: North America, Western Europe/Israel, and Australia/South Africa enrolled similar proportions of men, apolipoprotein E ε4 carriers, and participants with spouse study partners, whereas Asia, Eastern Europe/Russia, and South America/Mexico had lower proportions for these variables.
Cholesterol and metal ions in Alzheimer's disease.
Review
New
Impact
Lim et al., Ann Arbor, United States. In Chem Soc Rev, Nov 2014
For example, (a) cholesterol has been shown to be misregulated in AD-afflicted brains, and the aberrant activity of proteins (particularly, apolipoprotein E (ApoE) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (HMGR)) has been linked to cholesterol-related AD exacerbation; (b) dyshomeostasis of metal ions associated with misfolded proteins (i.e., amyloid-β (Aβ) aggregates) found in the brains of AD patients is shown to promote oxidative stress leading to the malfunction of multiple proteins, including cytochrome c oxidase (CcO), and Cu/Zn superoxide dismutase (SOD1); (c) metal ion misregulation has also been observed to disrupt the activity of proteins (e.g., HMGR, low-density lipoproteins (LDL)), required for cholesterol production and regulation.
Apolipoprotein E in Alzheimer's disease: an update.
Review
Impact
Hardy et al., Qingdao, China. In Annu Rev Neurosci, 2013
Apolipoprotein E (APOE) has been irrefutably recognized as the major genetic risk factor, with semidominant inheritance, for LOAD.
Review
Lau et al., Rockville, United States. In Unknown Journal, 0001
OBJECTIVE: We assessed four pharmacogenetic tests: 1) cytochrome P450, subfamily IIC, polypeptide 9 (CYP2C9), 2) vitamin K epoxide reductase subunit protein 1 (VKORC1), 3) apolipoprotein E (Apo E), and 4) methylenetetrahydrofolate reductase (MTHFR) for their associations with patient’s response to therapy with warfarin (CYP2C9 and VKORC1), statins (Apo E), or antifolate chemotherapy (MTHFR).
share on facebooktweetadd +1mail to friends