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J. Biol. Chem., Vol. 276, Issue 40, 37186-37193, October 5, 2001
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,,
,,,,, and**
From the Institutes of p53 tumor suppressor is a
transcription factor that functions, in part, through many of its
downstream target genes. We have identified a p53-inducible gene by
performing mRNA differential display on IW32 murine erythroleukemia
cells containing a temperature-sensitive p53 mutant allele,
tsp53Val-135. Sequence analysis of the
full-length cDNA revealed its identity as the mouse homologue of
the human thiamine transporter 1 (THTR-1). Induction of the mouse
THTR-1 (mTHTR-1) mRNA was detectable as early as 1 h at
32.5 °C; upon shifting back to 38.5 °C, mTHTR-1 transcript was
rapidly degraded with a half-life of less than 2 h. Elevation of
mTHTR-1 expression was found in DNA damage-induced normal mouse
embryonic fibroblast cells, but not in p53 Biochemistry and
Microbiology and Immunology, National Yang Ming University,
Shih-Pai, Taipei 112, Taiwan, the § Institute of
Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan, and the
¶ Department of Obstetrics and Gynecology, University of Michigan,
Ann Arbor, Michigan 48109
/
mouse embryonic fibroblast cells, suggesting that mTHTR-1 induction was
p53-dependent. A region within the first intron of the
mTHTR-1 gene bound to p53 and conferred the p53-mediated
transactivation. Furthermore, increased thiamine transporter activities
were found in cells overexpressing mTHTR-1 and under conditions of DNA
damage or p53 activation. Our findings indicate that p53 may be
involved in maintaining thiamine homeostasis through transactivation of THTR-1.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF179403 (cDNA) and AF224341 (genomic).
** To whom correspondence should be addressed. Tel.: 022-826-7126; Fax: 022-826-4843; E-mail: ffwang@ym.edu.tw.This article has been cited by other articles:
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  K. G. McLure, M. Takagi, and M. B. Kastan NAD+ Modulates p53 DNA Binding Specificity and Function Mol. Cell. Biol., November 15, 2004; 24(22): 9958 - 9967. [Abstract] [Full Text] [PDF]
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W. Bruins, E. Zwart, L. D. Attardi, T. Iwakuma, E. M. Hoogervorst, R. B. Beems, B. Miranda, C. T. M. van Oostrom, J. van den Berg, G. J. van den Aardweg, et al. Increased Sensitivity to UV Radiation in Mice with a p53 Point Mutation at Ser389 Mol. Cell. Biol., October 15, 2004; 24(20): 8884 - 8894. [Abstract] [Full Text] [PDF]
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 G. Fiucci, S. Beaucourt, D. Duflaut, A. Lespagnol, P. Stumptner-Cuvelette, A. Geant, G. Buchwalter, M. Tuynder, L. Susini, J.-M. Lassalle, et al. Siah-1b is a direct transcriptional target of p53: Identification of the functional p53 responsive element in the siah-1b promoter PNAS, March 9, 2004; 101(10): 3510 - 3515. [Abstract] [Full Text] [PDF]
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 K. Oishi, S. Hofmann, G. A. Diaz, T. Brown, D. Manwani, L. Ng, R. Young, H. Vlassara, Y. A. Ioannou, D. Forrest, et al. Targeted disruption of Slc19a2, the gene encoding the high-affinity thiamin transporter Thtr-1, causes diabetes mellitus, sensorineural deafness and megaloblastosis in mice Hum. Mol. Genet., November 1, 2002; 11(23): 2951 - 2960. [Abstract] [Full Text] [PDF]
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