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anti-Mouse (Murine) APOE Antibodies:
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Human Monoclonal APOE Primary Antibody for CyTOF, ELISA - ABIN258785
Wahrle, Jiang, Parsadanian, Hartman, Bales, Paul, Holtzman: Deletion of Abca1 increases Abeta deposition in the PDAPP transgenic mouse model of Alzheimer disease. in The Journal of biological chemistry 2005
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Human Polyclonal APOE Primary Antibody for IHC, WB - ABIN2774066
Ho, Niti, Yap, Kua, Ng: Metabolic syndrome and cognitive decline in chinese older adults: results from the singapore longitudinal ageing studies. in The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry 2008
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Human Polyclonal APOE Primary Antibody for ELISA, WB - ABIN543949
Christensen, Batterham, Mackinnon, Jorm, Mack, Mather, Anstey, Sachdev, Easteal: The association of APOE genotype and cognitive decline in interaction with risk factors in a 65-69 year old community sample. in BMC geriatrics 2008
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Human Polyclonal APOE Primary Antibody for IHC (p), ELISA - ABIN1997537
Li, Jiang, Qu, Yao, Cai, Chen, Peng: Hepatocyte nuclear factor 4? and downstream secreted phospholipase A2 GXIIB regulate production of infectious hepatitis C virus. in Journal of virology 2013
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Monoclonal APOE Primary Antibody for IHC (fro), ELISA - ABIN534094
Krul, Tikkanen, Schonfeld: Heterogeneity of apolipoprotein E epitope expression on human lipoproteins: importance for apolipoprotein E function. in Journal of lipid research 1989
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Human Monoclonal APOE Primary Antibody for FACS, IHC - ABIN968962
Karpouzis, Caridha, Tripsianis, Michailidis, Martinis, Veletza: Apolipoprotein E gene polymorphism in psoriasis. in Archives of dermatological research 2009
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Human Polyclonal APOE Primary Antibody for IHC - ABIN6713286
Park, Kim, Bae, Hong, Lee, Leem, Choi, Shin: Protective effect of the phosphodiesterase III inhibitor cilostazol on amyloid β-induced cognitive deficits associated with decreased amyloid β accumulation. in Biochemical and biophysical research communications 2011
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Human Polyclonal APOE Primary Antibody for IHC (p), ELISA - ABIN547420
Dodart, Marr, Koistinaho, Gregersen, Malkani, Verma, Paul: Gene delivery of human apolipoprotein E alters brain Abeta burden in a mouse model of Alzheimer's disease. in Proceedings of the National Academy of Sciences of the United States of America 2005
Human Monoclonal APOE Primary Antibody for ELISA, IP - ABIN4281146
Calero, García-Albert, Rodríguez-Martín, Veiga, Calero: A fast and cost-effective method for apolipoprotein E isotyping as an alternative to APOE genotyping for patient screening and stratification. in Scientific reports 2018
A loss of a single Src family kinase, Fgr or Lyn, reduced platelet-mediated monocyte recruitment in vitro and a significant reduction in the burden of atherosclerotic disease in Fgr(-/-) /ApoE(-/-) or Lyn(-/-) /ApoE(-/-) animals.
there is a predilection of low protein C-induced spontaneous atherothrombosis in Apoe(-/-) mice for the right coronary sinus.
analysis of the APOE( *)3-Leiden.glucokinase(+/-) (E3L.GK(+/-)) mouse reveals that it is a model of metabolic syndrome and diabetic complications
chronic high-fat and high-cholesterol diet intake in a mouse model of atherosclerosis (ApoE-/-) decreases the level of ceramides and glucosylceramide.
AnxA5 treatment attenuates the post-ischemic inflammatory response and ameliorates LV remodeling which improves cardiac function three weeks after MI-R injury in hypercholesterolemic ApoE*3-Leiden mice.
Here we report that Cnn2 KO also decreased calcification of the aortic valve in ApoE KO mice, an established model of Calcific aortic valve disease
ApoE role in the hepatic bile acid homeostasis.
aged females demonstrated a significant exacerbation of many of these shared transcripts in this APOE network, revealing a potential mechanism for increased AD susceptibility in females. This study has broad implications for microglial transcriptomic approaches and provides new insights into microglial pathways associated with different pathological aspects of aging and AD.
Augmentation of intracellular adenosine levels through ADK knockout in myeloid cells protects ApoE(-/-) mice against atherosclerosis by reducing foam cell formation via the epigenetic regulation of cholesterol trafficking.
ApoE and Fasl(gld) knockout C57BL/6 mice simultaneously exhibited systemic lupus erythematosus and atherosclerosis characteristics and endothelial cell injury.
Immune activation in response to hyperlipidemia in ApoE knockout mice could contribute to a wide range of inflammatory autoimmune diseases, including atherosclerosis.
These data point to up-regulation of endothelial BKCa channels and CB2 receptors in ApoE(-/-) arteries.
the potential function of Pin1 in smooth muscle cells (SMCs) and its contribution to abdominal aortic aneurysm (AAA) pathogenesis in ApoE(-/-) mice, was examined.
PSRC1 protects against the development of atherosclerosis and enhances the stability of plaques by modulating cholesterol transportation and inflammation in macrophages and the liver of apoE(-/-) mice.
our results in this study suggest that ApoE4 genotype specific PIP2 dyshomeostasis contributes to the development of Tau hyper-phosphorylation after blast TBI exposure, and that elevation of brain PIP2 levels by reducing synj1 expression may ameliorate TBI- associated Tauopathy in ApoE4 carriers.
Dietary fat modulates osteoblastic, osteoclastic,and lipoblastic differentiation, and activity in a background of AlphaPOE deficiency.
The results of this study reveal E4/Abca1(+/-) TBI mice have a distinct response to injury, and unique gene networks are associated with APOE isoform, Abca1 insufficiency and injury.
In the present study, it was investigated whether ticagrelor reduces oxidized lowdensity lipoprotein (oxLDL)induced endothelial cell apoptosis, an initial step for the development of atherosclerosis(AS), and alleviates AS in apolipoproteinEdeficient (ApoE/) mice by inhibiting the expression of proprotein convertase subtilisin/kexin type 9 (PCSK9)
ApoE does not function in protecting the brain from oxidative damage resulting from copper build-up in Wilson's disease, but may play a role in regulating copper accumulation in the brain.
Data indicate that ApoE is a classical complement cascade checkpoint inhibitor by binding to activated C1q and that the resulting C1q-ApoE complex emerges as a common player to impact brain inflammation and atherosclerosis.
ApoE and apoCIII on HDL interact to affect metabolism and coronary heart disease (CHD). ApoE promotes metabolic steps in reverse cholesterol transport and is associated with lower risk of CHD. ApoCIII, when coexisting with apoE on HDL, abolishes these benefits. Therefore, differences in metabolism of HDL subspecies pertaining to reverse cholesterol transport are reflected in differences in association with CHD.
astrocytes expressing E4 accumulate significantly more and smaller lipid droplets compared to E3 astrocytes.
The results showed that the APOE 3 allele was a protective factor for PD [ Parkinson disease ](OR = 0.90, 95% CI: 0.81-0.99; P = .04), whereas no significant differences in PD risk among all cases compared to controls were found for APOE 2 and 4. In Asian subgroups, the APOE 4 allele was shown to be a risk factor for PD [ Parkinson disease ]
Lipoprotein glomerulopathy (LPG)-associated apoE3 mutations R25C, R114C, and A152D induce protein misfolding, which may contribute to protein aggregation in glomerular capillaries. The thermodynamic destabilization and enhanced aggregation of both proline and non-proline mutations may constitute a common underlying mechanism behind the pathogenesis of LPG.
Dementia risk was significantly higher among participants at high or intermediate APOE risk compared with those at low APOE risk ..APOE genotype significantly modified the association between protective factors and dementia
Findings suggest a meaningful relationship between APOE genotype and psychiatric distress post-military-related traumatic brain injury
Our data show that APOE4 may be associated with lower bone formation as well as increased risk of osteoporosis and bone fractures, whereas APOE3 seems to decrease lowering BMD in postmenopausal women, and its presence seemed to lower the incidence of bone breaking in patients with osteoporosis.
Results provide independent validation that the APOE CGI holds lower DNA methylation levels in AD compared to control in frontal lobe but not cerebellar tissue. Data also indicate that the non-neuronal cells of the AD brain, which are mainly composed of glia, are the main contributors to the lower APOE DNA methylation observed in AD PMB.
Participants with ApoE4(e3/e4) allele had higher levels of LDL-C (p=0.010), independently of HbA1c. CONCLUSIONS: Females and subjects with suboptimal metabolic control had more adverse lipid profiles. ApoE4(e3/e4) alleles were associated with significantly higher LDL-C levels, independently of HbA1c
Apolipoprotein E genotypes among diverse middle-aged and older Latinos: Study of Latinos-Investigation of Neurocognitive Aging results.
Prior work has shown that beta-amyloid and Apolipoprotein E epsilon4 combine to influence memory decline in nondemented older adults. This study indicate that increasing age may further exacerbate these effects.
APOE rs7412 and rs429358 SNPs showed a statistically significant association for the risk of cervical spondylotic myelopathy in Indian population.
ApoE4 is the largest risk factor for Alzheimer disease (AD), and is an independent risk factor for coronary heart disease (CHD); ApoE4 is likely to be the bridge between AD and CHD
APOE-e4 allele is associated with Alzheimer disease risk in Jordanian population.
Apolipoprotein E region molecular signatures of Alzheimer's disease
ApoE4 is a risk factor for TDP-43 deposition in Alzheimer's disease.
age, sex and APOE genotype robustly identify high-risk groups for Alzheimer disease and all dementia; these groups can potentially be targeted for preventive interventions
These results highlight the importance of the LSR polymorphism and reveal the existence of complex molecular links between LSR and ApoE for the regulation of lipid levels, revealing potential new pathways of interest in type III hyperlipidemia and its involvement in cardiovascular disease pathology.
These findings evidenced a novel role of BDNF in the modulation of ApoE and cholesterol homeostasis in glial and neuronal cells.
Studied the association between chronic low-grade inflammation (C reactive protein levels) and risk of Alzheimer Disease (AD) in ApoE4 carrier genotypes.
we report the efficient creation of an APOE knockout rabbit by using zinc finger nucleases. The knockout rabbits had drastically elevated cholesterol and moderately increased triglyceride levels, mimicking symptoms in human heart disease.
These differentially expressed proteins associated with key mechanisms involved in atherosclerosis and signaling mechanisms related with vitamin E.
The molar ratio ApoE/ApoA-I is negatively correlated with the enzyme activity, and positively correlated with increases in the intima-media thickness of common carotid wall and cardiac dysfunction signs.
ApoE mimetic peptide reduces plasma lipid hydroperoxide content with a concomitant increase in HDL paraoxonase activity
The identification of disulphide-linked apoE dimers in cortical and hippocampal tissues represents a distinct structural difference between the apoE3 and apoE4 isoforms that may have functional consequences.
These data suggest that the -155T>A mutation in the promoter region of the porcine APOE gene is an important functional variant
Nonesterified fatty acids significantly inhibit the expression of ApoB100, ApoE, MTP, and LDLR, thereby decreasing the synthesis and assembly of VLDL and inducing TG accumulation in bovine hepatocytes.
Bovine apoE contents in triglyceride-rich lipoproteins are modulated by nutritional treatment and closely associated with triglyceride-rich lipoprotein metabolism
apoE-containing particles, which increased during the lactating stage, were not associated with HDL particles, and lipid-free forms were included in cow plasma
after calving the apolipoprotein B(100) mRNA synthesis was lower, whereas microsomal triglyceride transfer protein (MTP) and apolipoprotein E messenger RNA abundance were higher in the liver
The study found no coding variation within and between chimpanzee populations, suggesting that the maintenance of functionally diverse APOE polymorphisms is a unique feature of human evolution.
ApoE evolution and very likely the evolution of other apolipoproteins are influenced by feeding environment and diet of humans, chimpanzees and various other species.
In the hippocampus APOE protein levels were higher in good spatial performers than poor spatial performers animals
Allele frequencies of the ApoE gene found show that allele epsilon3 has one of the highest frequencies and epsilon4 allele one of the lowest compared to other population groups in the world
There was significantly more apoE immunoreactivity in the prefrontal cortex and hippocampus of aged animals compared to adult or middle-aged animals.
Chylomicron remnants and very low density lipoprotein (VLDL) remnants are rapidly removed from the circulation by receptor-mediated endocytosis in the liver. Apolipoprotein E, a main apoprotein of the chylomicron, binds to a specific receptor on liver cells and peripheral cells. ApoE is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. The APOE gene is mapped to chromosome 19 in a cluster with APOC1 and APOC2. Defects in apolipoprotein E result in familial dysbetalipoproteinemia, or type III hyperlipoproteinemia (HLP III), in which increased plasma cholesterol and triglycerides are the consequence of impaired clearance of chylomicron and VLDL remnants.
, apolipoprotein E3