title: Phenotypic reversion in analbuminemic rats due to an altered splicing mechanism.
abstract: Serum albumin is regarded as an important and indispensable protein, but analbuminemic rats established by Sumi Nagase in 1977 seems to exhibit few symptoms in spite of an almost total lack of albumin in the serum. The albumin gene of analbuminemic rats was found to have a seven-base-pair deletion in an intron, close to exon-intron junction, resulting in the formation of non-functional mRNA in hepatocytes. Immunostaining for albumin was negative in young analbuminemic rat hepatocytes, but a significant number of immunoreactive hepatocytes were observed in aged rats. The incidence of immunoreactive hepatocytes increased with aging. Surprisingly, many immunoreactive hepatocytes were observed after hepatocarcinogen treatment sometimes in large clusters. Albumin transcripts in analbuminemic rat liver after treatment with carcinogen, showed an altered pattern of exon-skipping. The altered albumin molecules thus synthesized accumulated in cellular organelles. Analbuminemic rats exhibited a high sensitivity in various organs to different types of carcinogens. Further challenges remain regarding the biology of analbuminemic rats.
authors.affiliation: Research Center for Innovative Oncology, National Cancer Center Hospital East, Chiba, Japan .
authors.forename: Hiroyasu
authors.initials: H
authors.lastname: Esumi
authors.forename: Takashi
authors.initials: T
authors.lastname: Sugimura
keywords: aging; albumin gene; alternative splicing; analbuminemic rat; carcinogenesis; exon skipping
references.citation: Jpn J Cancer Res. 1988 Jul;79(7):775-84
references.pmid: 3139593
references.citation: Science. 1979 Aug 10;205(4406):590-1
references.pmid: 451621
references.citation: Proc Natl Acad Sci U S A. 1991 Apr 1;88(7):2707-11
references.pmid: 2011581
references.citation: Biochem Biophys Res Commun. 1998 Oct 9;251(1):11-6
references.pmid: 9790899
references.citation: Jpn J Cancer Res. 1986 Feb;77(2):153-9
references.pmid: 3082826
references.citation: Cancer Res. 1982 Jan;42(1):306-8
references.pmid: 6172194
references.citation: Eur J Cell Biol. 1993 Aug;61(2):239-46
references.pmid: 8223714
references.citation: J Cell Sci. 2006 Jul 1;119(Pt 13):2635-41
references.pmid: 16787944
references.citation: Proc Natl Acad Sci U S A. 1982 Feb;79(3):734-8
references.pmid: 6950424
references.citation: Proc Natl Acad Sci U S A. 2005 Feb 22;102(8):2970-4
references.pmid: 15710887
references.citation: Eur J Pediatr. 2004 Nov;163(11):664-70
references.pmid: 15300429
references.citation: Biochem Biophys Res Commun. 1982 Jun 15;106(3):863-70
references.pmid: 6810889
references.citation: Proc Natl Acad Sci U S A. 1979 Sep;76(9):4370-4
references.pmid: 291970
references.citation: Biochem Biophys Res Commun. 1979 Apr 27;87(4):1191-9
references.pmid: 465033
references.citation: Proc Natl Acad Sci U S A. 1980 Jun;77(6):3215-9
references.pmid: 6932016
references.citation: Am J Med. 2006 Feb;119(2):181-2
references.pmid: 16443434
references.citation: Eur J Cell Biol. 1990 Dec;53(2):267-74
references.pmid: 2127918
references.citation: Cancer Res. 2004 Nov 1;64(21):7647-54
references.pmid: 15520162
references.citation: Proc Natl Acad Sci U S A. 1983 Jan;80(1):95-9
references.pmid: 6572011
references.citation: Br J Cancer. 1982 Mar;45(3):474-6
references.pmid: 7073941
references.citation: Ann N Y Acad Sci. 1983;417:31-8
references.pmid: 6200039
references.citation: Trends Biochem Sci. 2005 Jun;30(6):279-81
references.pmid: 15950867