A new functional domain of Bcl6 family that recruits histone deacetylases
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作者:
Zhang, H
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Chiba Univ, Grad Sch Med, Dept Dev Genet H2, Chuo Ku, Chiba 2608670, JapanChiba Univ, Grad Sch Med, Dept Dev Genet H2, Chuo Ku, Chiba 2608670, Japan
Zhang, H
[1
]
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Okada, S
[1
]
Hatano, M
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Chiba Univ, Grad Sch Med, Dept Dev Genet H2, Chuo Ku, Chiba 2608670, JapanChiba Univ, Grad Sch Med, Dept Dev Genet H2, Chuo Ku, Chiba 2608670, Japan
Hatano, M
[1
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Okabe, S
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Chiba Univ, Grad Sch Med, Dept Dev Genet H2, Chuo Ku, Chiba 2608670, JapanChiba Univ, Grad Sch Med, Dept Dev Genet H2, Chuo Ku, Chiba 2608670, Japan
Okabe, S
[1
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Tokuhisa, T
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Chiba Univ, Grad Sch Med, Dept Dev Genet H2, Chuo Ku, Chiba 2608670, JapanChiba Univ, Grad Sch Med, Dept Dev Genet H2, Chuo Ku, Chiba 2608670, Japan
Tokuhisa, T
[1
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[1] Chiba Univ, Grad Sch Med, Dept Dev Genet H2, Chuo Ku, Chiba 2608670, Japan
来源:
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
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2001年
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1540卷
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03期
The proto-oncogene Bc16 and its family gene. BAZF. encode a sequence-specific transcriptional repressor which contains the BTB/POZ domain in NH2-terminal region and zinc finger motifs in COOH-terminal region. The BTB/POZ domain and the middle portion of Bc16 and BAZF are known to display transrepressor activity. Since we have identified the identical 17-amino acid (aa) sequence in the middle portion of Bc16 and BAZF, the 17aa region may be another repressive domain of the middle portion. The reporter gene assay indicates that the 27aa sequence including the 17aa region recruits historic deacetylases to express transrepressor activity. Furthermore, overexpression of Bc16 or Bc16(POZ-) (Bc16 deleted with the BTB/POZ domain) induced apoptosis in NIH3T3 cells, and the apoptosis was inhibited by the addition of historic deacetylase inhibitor in the culture. However. apoptosis was not induced in NIH3T3 cells by overexpression of Bc16(POZ-) deleted with the 17aa region. These results indicate that the 17aa region in the middle portion of Bc16 is a functional domain of transrepressor activity and is responsible for inducibility of apoptosis in NIH3T3 cells. (C) 2001 Elsevier Science BN. All rights reserved.
机构:
Washington Univ, Sch Med, Howard Hughes Med Inst, Dept Med,Div Mol Oncol, St Louis, MO 63110 USAWashington Univ, Sch Med, Howard Hughes Med Inst, Dept Med,Div Mol Oncol, St Louis, MO 63110 USA
Chao, DT
;
Korsmeyer, SJ
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机构:Washington Univ, Sch Med, Howard Hughes Med Inst, Dept Med,Div Mol Oncol, St Louis, MO 63110 USA
机构:
Washington Univ, Sch Med, Howard Hughes Med Inst, Dept Med,Div Mol Oncol, St Louis, MO 63110 USAWashington Univ, Sch Med, Howard Hughes Med Inst, Dept Med,Div Mol Oncol, St Louis, MO 63110 USA
Chao, DT
;
Korsmeyer, SJ
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机构:Washington Univ, Sch Med, Howard Hughes Med Inst, Dept Med,Div Mol Oncol, St Louis, MO 63110 USA