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apoC-I and apoC-III (show APOC3 Proteins) inhibit lipolysis by displacing LPL (show LPL Proteins) from lipid emulsion particles. We also propose a role for these apolipoproteins in the irreversible inactivation of LPL (show LPL Proteins) by factors such as angptl4 (show ANGPTL4 Proteins).
Among white women, three single nucleotide polymorphisms (SNPs) (rs2075650 [TOMM40 (show TOMM40 Proteins)], rs4420638 [APOC1], and rs429358 [APOE (show APOE Proteins)]) 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 (show LCP1 Proteins) 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 (show LCP1 Proteins) 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 (show C9orf3 Proteins))C1 GG and AG carriers, APOE (show APOE Proteins) varepsilon4 carriers, insulin-degrading enzyme (IDE (show IDE Proteins)) TC carriers, and phosphatidylinositol 3-kinase (PI3KCB) GG carriers.
Common single-nucleotide polymorphism in the APOC1/APOE (show APOE Proteins) 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 (show TOMM40 Proteins)/APOE (show APOE Proteins)/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 (show SUCLA2 Proteins)-42 levels in CSF (show CSF2 Proteins).
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 (show EDNRB Proteins)) and apolipoprotein C1 (APOC1) genes have high sequence identity but differ in activity and tissue specificity.
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 (show TLR4 Proteins))response resembles that of LPS-binding protein (LBP (show LBP Proteins)) and depends on CD14 (show CD14 Proteins)/ Toll-like receptor 4 (show TLR4 Proteins) signaling.
present observations provide direct support for a potent specific inhibition of CETP (show CETP Proteins) by plasma apoCI in vivo
The apoC-I content of lipoprotein remnants may serve as an early marker of coronary artery disease risk.
TR4 (show NR2C2 Proteins) can also regulate apolipoprotein E (show APOE Proteins), C-I, and C-II gene expression via the TR4 (show NR2C2 Proteins) response element within the hepatic control region
apoC-I is a potent inhibitor of LPL (show LPL Proteins)-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 (show VLDLR Proteins) and apoCIII (show APOC3 Proteins) in mice
Endogenous apoC-I increases hyperlipidemia in apoE (show APOE Proteins)-knockout mice by stimulating VLDL production and inhibiting LPL (show LPL Proteins).
Cholesteryl ester transfer protein (show CETP Proteins) 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 (show HSD11B1 Proteins) 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 C-I
, apolipoprotein C1
, liver regeneration-related protein LRRG04