Disease relevance of APOA1

• High-density lipoprotein from hypercholesterolemic animals has peroxidized lipids and oligomeric apolipoprotein A-I: its putative role in atherogenesis [1].
• Regulation by estrogen of synthesis and secretion of apolipoprotein A-I in the chicken hepatoma cell line, LMH-2A [2].

High impact information on APOA1

• The expression of the apolipoprotein A-I (apo A-I) gene was investigated in the myelinating sciatic nerve [3].
• The apolipoprotein A-I gene is actively expressed in the rapidly myelinating avian peripheral nerve [3].
• Comparison of the rates of movement of triacyl[3H]glycerol, apolipoprotein B, apolipoprotein II, and apolipoprotein A-I through the ER and Golgi and of their secretion in nascent VLDL suggests that assembly of triacyglycerol with apolipoproteins occurs in the Golgi [4].
• Apolipoprotein A-I production by chicken granulosa cells [5].
• We propose that the ApoA-I-containing particles secreted by granulosa cells 1) support the growth of the rapidly growing germ cell, possibly by direct lipid transfer to the plasma membrane of the oocyte, and/or 2) deliver cholesteryl esters to the steroid-producing cells of the theca layer [5].

Biological context of APOA1

• The identity of the clone was confirmed by comparison with partial amino acid sequences for chicken apolipoprotein A-I [6].
• A full-length cDNA clone for the precursor form of chicken liver apolipoprotein A-I (apoA-I) was isolated by antibody screening of a chicken liver cDNA library in the expression vector lambda gt11 [6].
• Evolutionary distinct mechanisms regulate apolipoprotein A-I gene expression: differences between avian and mammalian apoA-I gene transcription control regions [7].
• The nucleotide (nt) sequence analysis of a full-length cDNA for chick apolipoprotein AI (Apo-AI) shows an open reading frame (ORF) of 792 nt, coding for a 264-aa protein [8].
• A mutant strain of chicken previously identified by a "recessive white skin" phenotype was found to have a profound deficiency in high density lipoprotein (HDL) and apolipoprotein A-I (apoA-I) [9].

Anatomical context of APOA1

• Rapid movement of newly synthesized chicken apolipoprotein AI to trans-Golgi network and its secretion in Madin-Darby canine kidney cells [10].
• Northern blot hybridization experiments showed that Apolipoprotein A-I (Apo A-I) mRNA is present at high concentration in chicken myotubes cultured in vitro, while it is virtually absent in fibroblasts and myoblasts [11].
• Plasma lipoproteins, tissue cholesterol overload, and skeletal muscle apolipoprotein A-I synthesis in the developing chick [12].
• Previous studies indicated that the differential expression of the chicken gene (ApoAI) encoding apolipoprotein AI (ApoAI) in the QMLA-29 and LMH cell lines may be the result of altered cis-elements and/or trans-acting factors [13].
• Band shift analyses of the -87 to +90 bp upstream DNA of ApoAI showed differences in the shifting patterns when nuclear proteins from LMH and liver cells were used [13].

Associations of APOA1 with chemical compounds

• Synthesis of apolipoprotein AI by peripheral tissues of the rooster. A possible mechanism of cellular cholesterol efflux [14].
• Both treatments produced several physical and chemical changes in the HDLs, i.e., formation of lipid peroxides, enlargement of HDL diameters, an increased exposure of the tryptophan groups of the apolipoprotein A-I to a more hydrophilic environment, formation of bityrosines, and cross-linking of apolipoprotein A-I [15].
• 3. Carotenoid content correlated best with protein content (principally apolipoprotein A-I) throughout the experiment [16].
• Analysis showed that the level of apoB mRNA was lower in cultures supplemented with octanoate than in the control cultures, but no significant changes were observed in the levels of apolipoprotein A-I, fatty acid synthase and 3-hydroxy-3-methylglutaryl-CoA reductase mRNA as a result of octanoate treatment [17].

Analytical, diagnostic and therapeutic context of APOA1

• To examine the cis-elements, LMH DNA was used as a template and the 5'-upstream region of ApoAI was PCR amplified [13].
• Towards gene therapy to enhance apolipoprotein AI expression [18].

References