ArticleThe Journal of clinical investigation1995
apo B gene knockout in mice results in embryonic lethality in homozygotes and neural tube defects, male infertility, and reduced HDL cholesterol ester and apo A-I transport rates in heterozygotes.
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 125 citations in OpenAlex.
- A humanized mouse model of APOB deficiency recapitulates hypobetalipoproteinemia.Journal of lipid research · 2026Article
- The intracellular chylomicron highway: novel insights into chylomicron biosynthesis, trafficking, and secretion.Current opinion in lipidology · 2025Review
- ApoM maintains cellular homeostasis between mitophagy and apoptosis by affecting the stability of Nnt mRNA through the Zic3-ApoM-Elavl2-Nnt axis during neural tube closure.Cell death & disease · 2025Article
- Where do obesity and male infertility collide?BMC medical genomics · 2024Article
- Aberrant lipid accumulation in the mouse visceral yolk sac resulting from maternal diabetes and obesity.Frontiers in cell and developmental biology · 2023Article
- Association between rare variants in specific functional pathways and human neural tube defects multiple subphenotypes.Neural development · 2020Article
- Cerebrovascular Changes and Neurodegeneration Related to Hyperlipidemia: Characteristics of the Human ApoB-100 Transgenic Mice.Current pharmaceutical design · 2020Article
- Nuclear envelope-localized torsinA-LAP1 complex regulates hepatic VLDL secretion and steatosis.The Journal of clinical investigation · 2019Article
- Sexual dysfunction and infertility in the male spina bifida patient.Translational andrology and urology · 2018Review
- Betaine in Inflammation: Mechanistic Aspects and Applications.Frontiers in immunology · 2018Review
- Characterization of cholesterol metabolism in Sertoli cells and spermatogenesis (Review).Molecular medicine reports · 2018Review
- Review
- Deficient Vitamin E Uptake During Development Impairs Neural Tube Closure in Mice Lacking Lipoprotein Receptor SR-BI.Scientific reports · 2017Article
- Mea6 controls VLDL transport through the coordinated regulation of COPII assembly.Cell research · 2016Article
- An apolipoprotein B100 mimotope prevents obesity in mice.Clinical science (London, England : 1979) · 2016Article
- Neural tube defects: from a proteomic standpoint.Metabolites · 2015Review
- Pathway Analysis: State of the Art.Frontiers in physiology · 2015Review
- A unique missense allele of BAF155, a core BAF chromatin remodeling complex protein, causes neural tube closure defects in mice.Developmental neurobiology · 2014Article
- Modeling anterior development in mice: diet as modulator of risk for neural tube defects.American journal of medical genetics. Part C, Seminars in medical genetics · 2013Review
- MicroRNA-122 influences the development of sperm abnormalities from human induced pluripotent stem cells by regulating TNP2 expression.Stem cells and development · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
apo B is a structural constituent of several classes of lipoprotein particles, including chylomicrons, VLDL, and LDL. To better understand the role of apo B in the body, we have used gene targeting in embryonic stem cells to create a null apo B allele in the mouse. Homozygous apo B deficiency led to embryonic lethality, with resorption of all embryos by gestational day 9. Heterozygotes showed an increased tendency to intrauterine death with some fetuses having incomplete neural tube closure and some live-born heterozygotes developing hydrocephalus. The majority of male heterozygotes were sterile, although the genitourinary system and sperm were grossly normal. Viable heterozygotes had normal triglycerides, but total, LDL, and HDL cholesterol levels were decreased by 37, 37, and 39%, respectively. Hepatic and intestinal apo B mRNA levels were decreased in heterozygotes, presumably contributing to the decreased LDL levels through decreased synthesis of apo B-containing lipoproteins. Kinetic studies indicated that heterozygotes had decreased transport rates of HDL cholesterol ester and apo A-I. As liver and intestinal apo A-I mRNA levels were unchanged, the mechanism for decreased apo A-I transport must be posttranscriptional. Heterozygotes also had normal cholesterol absorption and a normal response of the plasma lipoprotein pattern to chronic consumption of a high fat, high cholesterol, Western-type diet. In summary, we report a mouse model for apo B deficiency with several phenotypic features that were unexpected based on clinical studies of apo B-deficient humans, such as embryonic lethality in homozygotes and neural tube closure defects, male infertility, and a major defect in HDL production in heterozygotes. This model presents an opportunity to study the mechanisms underlying these phenotypic changes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.