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Association between APOC1 rs11568822 polymorphism and Alzheimer's disease risk can be explained by linkage disequilibrium with the APOE locus.
PPARgamma knockdown resulted in increased levels of TOMM40, APOE and APOC1 -mRNAs, showing the strongest impact on APOE transcript levels.
Collectively, these findings suggest that apoC1 and apoE have redundant functions in the hepatitis C virus (HCV) infection and morphogenesis.
the relationship between two variants of apoC1 and the risk of polycystic ovary syndrome, evaluated the genotypic effects on clinical, hormonal and metabolic indexes and plasma platelet-activating factor acetylhydrolase (PAF-AH) activity, was investigated.
Performance metrics were used to select SNPs in stage 1, which were then genotyped to another dataset (stage 2). Four SNPs (CPXM2 rs2362967, APOC1 rs4420638, ZNF521 rs7230380, and rs12965520) were identified for LOAD by both traditional P-values (without correcting for multiple tests) and performance metrics.
ApoC-I polymorphism might be one of the genetic factors of longevity in Bama; the ApoC-I rs4420638 and rs584007 SNPs are associated with serum triglycerides and high-density lipoprotein-cholesterol levels in the longevous population
Among white women, three single nucleotide polymorphisms (SNPs) (rs2075650 [TOMM40], rs4420638 [APOC1], and rs429358 [APOE]) were significantly associated with survival to 90 years after correction for multiple testing (p < .001); rs4420638 and rs429358 were also significantly associated with healthy aging (p = .02). In African American women, no SNP was associated with longevity. In Hispanic women, 7 SNPs in linkage dise
APOC1 expression induces glomerulosclerosis, potentially by increasing the cytokine response in macrophages.
apoC-I inhibited in situ LPL activity in adipocytes in both a concentration- and time-dependent manner. There was no change in postprandial WAT apoC-I secretion. WAT apoC-I secretion may inhibit WAT LPL activity and promote delayed chylomicron clearance in overweight and obese subjects
People with allelic variation in four genes related to cardiovascular diseases and metabolism were more likely to die: apolipoprotein (APO)C1 GG and AG carriers, APOE varepsilon4 carriers, insulin-degrading enzyme (IDE) TC carriers, and phosphatidylinositol 3-kinase (PI3KCB) GG carriers.
Common single-nucleotide polymorphism in the APOC1/APOE region, previously found to be associated with protective levels of cholesterol and lower cardiovascular risk, may be associated with ideal health.
These findings indicated that variants in TOMM40/APOE/APOC1 region might be associated with human longevity. Further studies are needed to identify the causal genetic variants influencing human longevity.
These results suggest that ApoC-I peptides may be a potential diagnostic biomarker and therapeutic approach for breast cancer.
APOC1 SNP is associated with the A beta-42 levels in CSF.
This sbioinformatics analysis explored the shared genetic etiology underlying Type 2 Diabetes and Alzheimer's Disease on SNP level, gene level, and pathway level. Six SNPs on APOC1 gene.
The endogenous retroviral promoters (LTRs) of the human endothelin B receptor (EDNRB) and apolipoprotein C1 (APOC1) genes have high sequence identity but differ in activity and tissue specificity.
The ability of apoC1 to inhibit CETP activity is impaired in patients with diabetes. Glycation of apoC1 leads to a change in its electrostatic properties that might account, at least in part, for a loss of constitutive CETP inhibition and an increase in plasma CETP activity in patients with diabetes.
APOE e4 allele status is associated with dementia and severity of Alzheimer's disease pathologic features in Parkinson disease.
Data indicate that apolipoprotein C-I (APOC1) rs11568822 polymorphism was associated with increased Alzheimer's disease (AD) risk in Caucasians, Asians and Caribbean Hispanics, but not in African Americans.
Helical domains that mediate lipid solubilization and ABCA1-specific cholesterol efflux in apolipoproteins C-I and A-II
Apolipoprotein C-I was significantly increased in obese mice plasma.
The absence of ApoC-I results in impaired memory functions, which is, together with previous data, suggestive of an important, bell-shaped gene-dose dependent role for ApoC-I in appropriate brain functioning
Data show that the stimulating effect of apoCI on the lipopolysaccharide (LPS)response resembles that of LPS-binding protein (LBP) and depends on CD14/ Toll-like receptor 4 signaling.
regulated expression of gene cluster in macrophages
present observations provide direct support for a potent specific inhibition of CETP by plasma apoCI in vivo
The apoC-I content of lipoprotein remnants may serve as an early marker of coronary artery disease risk.
TR4 can also regulate apolipoprotein E, C-I, and C-II gene expression via the TR4 response element within the hepatic control region
apoC-I is a potent inhibitor of LPL-mediated triglyceride lipolysis
irrespective of receptor-mediated remnant clearance by the liver, liver-specific expression of recombinant human apoCI causes hypertriglyceridemia in the absence of the VLDLr and apoCIII in mice
Endogenous apoC-I increases hyperlipidemia in apoE-knockout mice by stimulating VLDL production and inhibiting LPL.
Knockout mice show significant increases in the hepatic content of cholesteryl esters and triglycerides and in biliary cholesterol concentration.
Systemic apoCI increases atherosclerosis, probably by inducing hyperlipidemia, in the absence of ApoE
Data suggest that apoC-I binds free fatty acids (FFA), thereby reducing the blood FFA for uptake by cells, and this mechanism can serve as an additional mechanism for the resistance to obesity and the cutaneous abnormalities of APOC1(+/+) mice.
apoCI is crucially involved in lipopolysaccharide(LPS)-induced atherosclerosis in apoe-/- mice, which mainly relates to an increased inflammatory response toward LPS
apoCI is a novel inhibitor of the scavenger receptor BI -mediated uptake of HDL cholesterol by hepatocytes; apoCI is a determinant for the plasma levels and size of HDL in vivo.
apoC-I and apoC-III inhibit lipolysis by displacing LPL from lipid emulsion particles. We also propose a role for these apolipoproteins in the irreversible inactivation of LPL by factors such as angptl4.
Cholesteryl ester transfer protein is the sole major determinant of cholesteryl ester transfer in normolipidemic rabbit plasma as a result of the inability of rabbit apoCI to change HDL electronegativity.
The protein encoded by this gene is a member of the apolipoprotein C1 family. This gene is expressed primarily in the liver, and it is activated when monocytes differentiate into macrophages. A pseudogene of this gene is located 4 kb downstream in the same orientation, on the same chromosome. This gene is mapped to chromosome 19, where it resides within a apolipoprotein gene cluster. Alternatively spliced transcript variants have been found for this gene, but the biological validity of some variants has not been determined.
, apolipoprotein C1
, liver regeneration-related protein LRRG04
, apolipoprotein C-I
, Apolipoprotein C-I