Published in Volume
81, Issue 2 (February 1988)
J Clin Invest. 1988;81(2):590–595.
doi:10.1172/JCI113357.
Copyright ©
1988, The American Society for
Clinical Investigation.
Research Article
Homozygous hypobetalipoproteinemia: a disease distinct from abetalipoproproteinemia at the molecular level.
R S Ross, R E Gregg, S W Law, J C Monge, S M Grant, K Higuchi, T J Triche, J Jefferson and H B Brewer, Jr
Molecular Disease Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892.
Published February 1988
apoB DNA, RNA, and protein from two patients with homozygous hypobetalipoproteinemia (HBL) were evaluated and compared with normal individuals. Southern blot analysis with 10 different cDNA probes revealed a normal gene without major insertions, deletions, or rearrangements. Northern and slot blot analyses of total liver mRNA from HBL patients documented a normal size apoB mRNA that was present in greatly reduced quantities. ApoB protein was detected within HBL hepatocytes utilizing immunohistochemical techniques; however, it was markedly reduced in quantity when compared with control samples. No apoB was detectable in the plasma of HBL individuals with an ELISA assay. These data are most consistent with a mutation in the coding portion of the apoB gene in HBL patients, leading to an abnormal apoB protein and apoB mRNA instability. These results are distinct from those previously noted in abetalipoproteinemia, which was characterized by an elevated level of hepatic apoB mRNA and accumulation of intracellular hepatic apoB protein.
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