TY - JOUR
T1 - Molecular cloning and chromosomal mapping of mouse intronless myc gene acting as a potent apoptosis inducer
AU - Sugiyama, Akinori
AU - Noguchi, Kohji
AU - Kitanaka, Chifumi
AU - Katou, Naoko
AU - Tashiro, Fumio
AU - Ono, Takeo
AU - Yoshida, Michihiro C.
AU - Kuchino, Yoshiyuki
N1 - Funding Information:
We thank Drs T. Tsuruo and N. Fujita (Tokyo University) for the gift of pcDNA3/3′HA and pCGNBL vector plasmids. This work was supported by a Grant-in-Aid from the Ministry of Health and Welfare of Japan for the second-term Comprehensive 10-Year Strategy for Cancer Control to YK, and by grants from the Ministry of Education, Science and Culture of Japan for cancer research to KN and YK.
PY - 1999/1/21
Y1 - 1999/1/21
N2 - Our previous findings suggest that the activation of the rat intronless myc gene provides a selective advantage in tumor suppression through apoptosis induction. In the present study, to examine whether intronless myc gene acting as an apoptosis inducer is evolutionarily conserved in mammalian cells, we isolated the mouse intronless myc gene and characterized it. A sequence analysis demonstrated that mouse intronless myc gene, ms-myc, has a linearly opened translatable frame consisting of 1293 bp with 90% homology with that of rat s-myc. The chromosomal locus of ms-myc was identified on chromosome 19B by a fluorescent in situ hybridization (FISH) analysis. Gene transfection experiments showed that the transient overexpression of ms-Myc with transactivation activity effectively induces cell death in a wild-type p53-independent manner. In addition, cells stably expressing transfected ms- myc became more susceptible to apoptosis induced by genotoxic stress such as UV-irradiation and hydrogen peroxide compared with untransfected control cells. These observations suggest that the rodents commonly contain an s- myc-type of intronless myc gene with apoptosis-inducing activity.
AB - Our previous findings suggest that the activation of the rat intronless myc gene provides a selective advantage in tumor suppression through apoptosis induction. In the present study, to examine whether intronless myc gene acting as an apoptosis inducer is evolutionarily conserved in mammalian cells, we isolated the mouse intronless myc gene and characterized it. A sequence analysis demonstrated that mouse intronless myc gene, ms-myc, has a linearly opened translatable frame consisting of 1293 bp with 90% homology with that of rat s-myc. The chromosomal locus of ms-myc was identified on chromosome 19B by a fluorescent in situ hybridization (FISH) analysis. Gene transfection experiments showed that the transient overexpression of ms-Myc with transactivation activity effectively induces cell death in a wild-type p53-independent manner. In addition, cells stably expressing transfected ms- myc became more susceptible to apoptosis induced by genotoxic stress such as UV-irradiation and hydrogen peroxide compared with untransfected control cells. These observations suggest that the rodents commonly contain an s- myc-type of intronless myc gene with apoptosis-inducing activity.
KW - FISH analysis
KW - Molecular evolution
KW - Myc Family gene
KW - Programmed cell death
KW - Transactivation factor
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U2 - 10.1016/S0378-1119(98)00547-2
DO - 10.1016/S0378-1119(98)00547-2
M3 - Article
C2 - 9931502
AN - SCOPUS:0033590617
VL - 226
SP - 273
EP - 283
JO - Gene
JF - Gene
SN - 0378-1119
IS - 2
ER -