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anti-Human Apolipoprotein C-II Antibodies:
anti-Rat (Rattus) Apolipoprotein C-II Antibodies:
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the apoc2 mutant zebrafish is a robust and versatile animal model to study hypertriglyceridemia.
Results from this exploratory analysis suggest that regulatory element methylation levels within the larger TOMM40 (show TOMM40 Antibodies)-APOE (show APOE Antibodies)-APOC2 gene region correlate with AD-related biomarkers and TOMM40 (show TOMM40 Antibodies) or APOE (show APOE Antibodies) gene expression in AD.
Triglyceride-raising variant alleles of the APOC2 encoding apo (show C9orf3 Antibodies) C-II, associated with clinical Cardiovascular endpoints.
The results demonstrate the important role of both intra- and inter-subunit charge interactions in stabilizing apoC-II amyloid fibrils, a process that may be a key factor in determining the general ability of proteins to form amyloid fibrils.
The results highlight the importance of charge-pair interactions within the apoC-II fibril core
Conformational rearrangement of apoC-II at lipoprotein surfaces promotes interaction with LPL (show LCP1 Antibodies).
Large deletion in APOC2 caused by Alu-Alu homologous recombination is associated with with apolipoprotein C-II deficiency.
No APOC2 mutations were identified in a cohort of patients with diabetic lipemia.
Six apolipoproteins (APOA1 (show APOA1 Antibodies), APOA2 (show APOA2 Antibodies), APOB (show APOB Antibodies), APOC2, APOC3 (show APOC3 Antibodies), and APOE (show APOE Antibodies)) were able to differentiate bladder cancer from hernia. SAA4 (show SAA4 Antibodies) was significantly increased in bladder cancer subgroups, whereas ProEGF was significantly decreased in bladder cancer subgroups.
STAT1 (show STAT1 Antibodies) bound on multienhancer 2 cooperates with RXRalpha (show RXRA Antibodies) located on apoCII promoter and upregulates apoCII expression only in macrophages.
Mutations in GPIHBP1 (show GPIHBP1 Antibodies) are rare but the associated clinical phenotype of hypertriglyceridaemia is severe
A novel mouse model of apoC-II deficiency was created with an apoC-II peptide that reverses the hypertriglyceridemia.
Data show that apoC-II and LPL (show LPL Antibodies) mRNAs correlate temporally and geographically with surfactant lipid synthesis in preparation for birth and suggest that fatty acid recruitment from the circulation by apoC-II-activated LPL (show LPL Antibodies) is modulated by apoC-II secretion.
TR4 (show NR2C2 Antibodies) can also regulate apolipoprotein E (show APOE Antibodies), C-I, and C-II gene expression via the TR4 (show NR2C2 Antibodies) response element within the hepatic control region
This gene encodes a lipid-binding protein belonging to the apolipoprotein gene family. The protein is secreted in plasma where it is a component of very low density lipoprotein. This protein activates the enzyme lipoprotein lipase, which hydrolyzes triglycerides and thus provides free fatty acids for cells. Mutations in this gene cause hyperlipoproteinemia type IB, characterized by hypertriglyceridemia, xanthomas, and increased risk of pancreatitis and early atherosclerosis. This gene is present in a cluster with other related apolipoprotein genes on chromosome 19. Naturally occurring read-through transcription exists between this gene and the neighboring upstream apolipoprotein C-IV (APOC4) gene.
, apolipoprotein C2