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Gene Review

Apobec1  -  apolipoprotein B mRNA editing enzyme,...

Mus musculus

Synonyms: Apolipoprotein B mRNA-editing enzyme 1, C->U-editing enzyme APOBEC-1
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Disease relevance of Apobec1

  • In contrast, in apoE-/- mice, inactivation of apobec-1 caused a massive increase (from <0.5 to 55.5+/-16.4 mg/dL) in plasma apoB-100 concentration but an approximately 55% reduction in hypercholesterolemia due to partial amelioration of the marked VLDL+IDL elevation [1].
  • Apobec-1 protects intestine from radiation injury through posttranscriptional regulation of cyclooxygenase-2 expression [2].
  • A recent report showing induction of DNA mutations in Escherichia coli by overexpression of AID, Apobec-1, and related members of the RNA-editing cytidine deaminase family suggested that they may directly modify deoxycytidine in DNA in mammalian cells (DNA-editing model) [3].
  • However, when the catalytic subunit of the editing enzyme complex, APOBEC-1, was overexpressed in transgenic mice and rabbits, numerous cytidines in the apoB mRNA and in a novel mRNA, NAT1, were aberrantly hyperedited, and the animals developed liver dysplasia and hepatocellular carcinomas [4].
  • Promoter-luciferase reporter constructions using regions flanking exon A and exon 1 of the rat apobec-1 gene identified two functional regions upstream of exon 1 that independently promote luciferase expression in transfected hepatoma and colon cancer cells [5].
  • Intestinal adenomas from compound Apc(min/+) apobec-1(-/-) mice showed a <2-fold increase in Cox-2 mRNA abundance and reduced prostaglandin E(2) content compared with adenomas from the parental Apc(min/+) strain [6].

High impact information on Apobec1


Biological context of Apobec1


Anatomical context of Apobec1


Associations of Apobec1 with chemical compounds


Regulatory relationships of Apobec1


Other interactions of Apobec1

  • Alternative mRNA splicing and differential promoter utilization determine tissue-specific expression of the apolipoprotein B mRNA-editing protein (Apobec1) gene in mice. Structure and evolution of Apobec1 and related nucleoside/nucleotide deaminases [19].
  • We conclude that in the absence of a functioning LDL receptor, hepatic overexpression of Apobec1 is highly efficient in lowering plasma apoB-100 levels, leading to the almost complete elimination of LDL particles and a reduction in LDL cholesterol and cholesteryl ester content [16].
  • Hepatic apobec-1 complementation factor mRNA and protein abundance were significantly decreased, whereas apobec-1 mRNA and protein abundance remained unchanged [20].
  • Hepatic ACF mRNA and protein abundance decreased in Pax8(-/-) mice, with restoration after thyroid hormone administration, whereas apobec-1 mRNA and protein abundance were unchanged [21].
  • TP ligands, including COX-1 (but not COX-2)-derived TxA2, promote initiation and early progression of atherogenesis in Apobec-1/LDLR DKOs but appear unimportant in the maintenance of established disease [22].

Analytical, diagnostic and therapeutic context of Apobec1


  1. Phenotype interaction of apobec-1 and CETP, LDLR, and apoE gene expression in mice: role of apoB mRNA editing in lipoprotein phenotype expression. Nakamuta, M., Taniguchi, S., Ishida, B.Y., Kobayashi, K., Chan, L. Arterioscler. Thromb. Vasc. Biol. (1998) [Pubmed]
  2. Apobec-1 protects intestine from radiation injury through posttranscriptional regulation of cyclooxygenase-2 expression. Anant, S., Murmu, N., Houchen, C.W., Mukhopadhyay, D., Riehl, T.E., Young, S.G., Morrison, A.R., Stenson, W.F., Davidson, N.O. Gastroenterology (2004) [Pubmed]
  3. RNA-editing cytidine deaminase Apobec-1 is unable to induce somatic hypermutation in mammalian cells. Eto, T., Kinoshita, K., Yoshikawa, K., Muramatsu, M., Honjo, T. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  4. Two efficiency elements flanking the editing site of cytidine 6666 in the apolipoprotein B mRNA support mooring-dependent editing. Hersberger, M., Innerarity, T.L. J. Biol. Chem. (1998) [Pubmed]
  5. Cloning and characterization of the rat apobec-1 gene: a comparative analysis of gene structure and promoter usage in rat and mouse. Hirano, K., Min, J., Funahashi, T., Davidson, N.O. J. Lipid Res. (1997) [Pubmed]
  6. Deletion of the AU-rich RNA binding protein Apobec-1 reduces intestinal tumor burden in Apc(min) mice. Blanc, V., Henderson, J.O., Newberry, R.D., Xie, Y., Cho, S.J., Newberry, E.P., Kennedy, S., Rubin, D.C., Wang, H.L., Luo, J., Davidson, N.O. Cancer Res. (2007) [Pubmed]
  7. Mammalian RNA-dependent deaminases and edited mRNAs. Maas, S., Melcher, T., Seeburg, P.H. Curr. Opin. Cell Biol. (1997) [Pubmed]
  8. A novel translational repressor mRNA is edited extensively in livers containing tumors caused by the transgene expression of the apoB mRNA-editing enzyme. Yamanaka, S., Poksay, K.S., Arnold, K.S., Innerarity, T.L. Genes Dev. (1997) [Pubmed]
  9. DNA double-strand breaks: prior to but not sufficient in targeting hypermutation. Bross, L., Muramatsu, M., Kinoshita, K., Honjo, T., Jacobs, H. J. Exp. Med. (2002) [Pubmed]
  10. Hepatic gene expression profiling reveals perturbed calcium signaling in a mouse model lacking both LDL receptor and Apobec1 genes. Dutta, R., Singh, U., Li, T.B., Fornage, M., Teng, B.B. Atherosclerosis (2003) [Pubmed]
  11. Involvement of a chaperone regulator, Bcl2-associated athanogene-4, in apolipoprotein B mRNA editing. Lau, P.P., Chan, L. J. Biol. Chem. (2003) [Pubmed]
  12. Complete phenotypic characterization of apobec-1 knockout mice with a wild-type genetic background and a human apolipoprotein B transgenic background, and restoration of apolipoprotein B mRNA editing by somatic gene transfer of Apobec-1. Nakamuta, M., Chang, B.H., Zsigmond, E., Kobayashi, K., Lei, H., Ishida, B.Y., Oka, K., Li, E., Chan, L. J. Biol. Chem. (1996) [Pubmed]
  13. Targeted disruption of the mouse apobec-1 gene abolishes apolipoprotein B mRNA editing and eliminates apolipoprotein B48. Hirano, K., Young, S.G., Farese, R.V., Ng, J., Sande, E., Warburton, C., Powell-Braxton, L.M., Davidson, N.O. J. Biol. Chem. (1996) [Pubmed]
  14. Apolipoprotein B RNA editing enzyme-deficient mice are viable despite alterations in lipoprotein metabolism. Morrison, J.R., Pászty, C., Stevens, M.E., Hughes, S.D., Forte, T., Scott, J., Rubin, E.M. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  15. Non-redundancy of cytidine deaminases in class switch recombination. Fugmann, S.D., Rush, J.S., Schatz, D.G. Eur. J. Immunol. (2004) [Pubmed]
  16. Effective lowering of plasma, LDL, and esterified cholesterol in LDL receptor-knockout mice by adenovirus-mediated gene delivery of ApoB mRNA editing enzyme (Apobec1). Teng, B., Ishida, B., Forte, T.M., Blumenthal, S., Song, L.Z., Gotto, A.M., Chan, L. Arterioscler. Thromb. Vasc. Biol. (1997) [Pubmed]
  17. Production of rabbit polyclonal antibody against apobec-1 by genetic immunization. Yeung, S.C., Anderson, J., Kobayashi, K., Oka, K., Chan, L. J. Lipid Res. (1997) [Pubmed]
  18. Hepatic secretion of small lipoprotein particles in apobec-1-/- mice is regulated by the LDL receptor. Nassir, F., Xie, Y., Patterson, B.W., Luo, J., Davidson, N.O. J. Lipid Res. (2004) [Pubmed]
  19. Alternative mRNA splicing and differential promoter utilization determine tissue-specific expression of the apolipoprotein B mRNA-editing protein (Apobec1) gene in mice. Structure and evolution of Apobec1 and related nucleoside/nucleotide deaminases. Nakamuta, M., Oka, K., Krushkal, J., Kobayashi, K., Yamamoto, M., Li, W.H., Chan, L. J. Biol. Chem. (1995) [Pubmed]
  20. The peroxisome proliferator-activated receptor alpha (PPARalpha) agonist ciprofibrate inhibits apolipoprotein B mRNA editing in low density lipoprotein receptor-deficient mice: effects on plasma lipoproteins and the development of atherosclerotic lesions. Fu, T., Mukhopadhyay, D., Davidson, N.O., Borensztajn, J. J. Biol. Chem. (2004) [Pubmed]
  21. Thyroid hormone regulates hepatic triglyceride mobilization and apolipoprotein B messenger ribonucleic Acid editing in a murine model of congenital hypothyroidism. Mukhopadhyay, D., Plateroti, M., Anant, S., Nassir, F., Samarut, J., Davidson, N.O. Endocrinology (2003) [Pubmed]
  22. Cyclooxygenases, thromboxane, and atherosclerosis: plaque destabilization by cyclooxygenase-2 inhibition combined with thromboxane receptor antagonism. Egan, K.M., Wang, M., Fries, S., Lucitt, M.B., Zukas, A.M., Puré, E., Lawson, J.A., FitzGerald, G.A. Circulation (2005) [Pubmed]
  23. Apolipoprotein B mRNA-editing protein induces hepatocellular carcinoma and dysplasia in transgenic animals. Yamanaka, S., Balestra, M.E., Ferrell, L.D., Fan, J., Arnold, K.S., Taylor, S., Taylor, J.M., Innerarity, T.L. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  24. Tissue-specific inhibition of apolipoprotein B mRNA editing in the liver by adenovirus-mediated transfer of a dominant negative mutant APOBEC-1 leads to increased low density lipoprotein in mice. Oka, K., Kobayashi, K., Sullivan, M., Martinez, J., Teng, B.B., Ishimura-Oka, K., Chan, L. J. Biol. Chem. (1997) [Pubmed]
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