John Elovson

TL;DR: It is proposed that only a single copy of B-48 is required for V LDL assembly in rat liver, unless nascent hepatic VLDL contain additional apoB peptides which are uniformly lost from the plasma VLDl particles when they are analyzed.

TL;DR: Kinetic analysis suggests that high mannose LPL disappears with a half-life of t0.5 = 40 min in both fed and fasted rats, indicating that the redistribution of LPL mass during feeding/fasting does not arise by differential retention within ER, and the fractional catabolic rate of complex LPL within the Golgi/post-Golgi secretory compartment can be calculated to be 3.5-fold greater in fasting.

TL;DR: The complete amino acid sequence of the liver-synthesized apolipoprotein B (apoB) species, apoB 100, has been derived from cloned cDNA and Cysteine is clustered in the N-terminal 1/10 of the protein, suggesting the presence of a stabilized tertiary structure in this part of the molecule.

TL;DR: Kinetic tracer experiments show that rat PI and PIII are present on separate VLDL particles, and that the declining PIII-to-PI/II ratios in IDL and LDL may be attributed to the more rapid turnover of P III-containing lipoproteins at all levels, particularly within the LDL density range.

TL;DR: A 20-fold increase in placental apoB mRNA concentrations during the last 48 hr of pregnancy suggests a specific role for this organ in maternal-fetal lipid transport immediately prior to parturition, and Pulse-labeling experiments using 21-day fetal tissue slices showed that the liver synthesizes both apOB-100 (B-PI) and apo B-48 (B -PIII) albeit in somewhat different ratios than the adult organ.