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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).
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.
The ability of apoC1 to inhibit CETP (show CETP Proteins) 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 (show CETP Proteins) inhibition and an increase in plasma CETP (show CETP Proteins) activity in patients with diabetes.
APOE (show APOE Proteins) 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 (show ABCA1 Proteins)-specific cholesterol efflux in apolipoproteins C-I and A-II
apoC-I and apoC-III (show APOC3 Proteins) inhibit lipolysis by displacing LPL (show LCP1 Proteins) from lipid emulsion particles. We also propose a role for these apolipoproteins in the irreversible inactivation of LPL (show LCP1 Proteins) by factors such as angptl4 (show ANGPTL4 Proteins).
Following regression analysis adjusted by collection center, gender, duration of diabetes, and average HbA1c, two SNPs were significantly associated with DN. rs4420638 in the APOC1 region and rs1532624 in CETP (show CETP Proteins).
Linkage disequilibrium between APOC1 and TOMM40 (show TOMM40 Proteins) is found in patients with primary progressive aphasia but not in controls or patients with frontotemporal dementia.
Increased white adipose tissue apoC-I secretion in obese women is associated with delayed postprandial dietary fat clearance mediated by increased triglyceride rich apoC-I.
The plasma level of apoC-I was significantly increased in obese individuals compared with healthy individuals.
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).
Systemic apoCI increases atherosclerosis, probably by inducing hyperlipidemia, in the absence of ApoE (show APOE 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