title: Regulatory mechanisms of human and mouse telomerase reverse transcriptase gene transcription: distinct dependency on c-Myc.
abstract: Telomerase-a complex ribonucleoprotein enzyme-synthesizes telomeric repeats to avoid telomere loss that accompanies cell division and chromosomal replication. Expression of telomerase is detectable in embryonic cells and cancer cells, but not in normal human cells. On the other hand, in mice, substantial expression of telomerase is detected in normal cells and tissues as well as in immortalized cells. These results suggest that the regulatory mechanisms of telomerase activity in humans and mice differ. Considering these results along with the fact that the expression of the telomerase reverse transcriptase (TERT) gene is a rate-limiting step for telomerase activity, we compared transcriptional regulatory mechanisms of both the species. A series of luciferase assays and RT-PCR analyses demonstrated that c-Myc, a dominant transactivator for human TERT (hTERT), is not involved in the regulation of mouse TERT (mTERT). These results suggest that distinct molecules and pathways are involved in the process of immortalization and tumorigenesis in human and mouse cells.
authors.affiliation: Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University, Fukuoka, 812-8581, Japan.
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Fujiki
authors.forename: Miyako
authors.initials: M
authors.lastname: Udono
authors.forename: Keishi
authors.initials: K
authors.lastname: Kadooka
authors.forename: Shuntaro
authors.initials: S
authors.lastname: Yamashita
authors.forename: Takumi
authors.initials: T
authors.lastname: Miura
authors.forename: Sanetaka
authors.initials: S
authors.lastname: Shirahata
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Katakura
references.citation: Nucleic Acids Res. 2000 Feb 1;28(3):669-77
references.pmid: 10637317
references.citation: Cancer Res. 1999 Dec 1;59(23):5917-21
references.pmid: 10606235
references.citation: Oncogene. 1999 Feb 4;18(5):1219-26
references.pmid: 10022128
references.citation: Proc Natl Acad Sci U S A. 2001 Mar 27;98(7):3826-31
references.pmid: 11274400
references.citation: Gene. 1999 May 17;232(1):97-106
references.pmid: 10333526
references.citation: Mol Cell Biol. 2005 Sep;25(18):8037-43
references.pmid: 16135795
references.citation: Oncogene. 2000 Mar 9;19(11):1485-90
references.pmid: 10723141
references.citation: Cancer Res. 1999 Feb 1;59(3):551-7
references.pmid: 9973199
references.citation: Cancer Res. 1998 Apr 1;58(7):1558-61
references.pmid: 9537264
references.citation: Genes Dev. 1998 Jun 15;12(12):1769-74
references.pmid: 9637678
references.citation: Cancer Res. 1998 Feb 15;58(4):622-5
references.pmid: 9485011
references.citation: Cancer Res. 1999 Feb 15;59(4):826-30
references.pmid: 10029071
references.citation: Hum Mol Genet. 1997 Nov;6(12):2011-9
references.pmid: 9328464
references.citation: Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10471-6
references.pmid: 9724727
references.citation: Cell. 1997 Aug 22;90(4):785-95
references.pmid: 9288757
references.citation: Cancer Res. 2000 Apr 15;60(8):2116-21
references.pmid: 10786671
references.citation: Science. 1997 Aug 15;277(5328):955-9
references.pmid: 9252327
references.citation: J Biol Chem. 2001 Jun 22;276(25):22016-23
references.pmid: 11279234