The HBP1 transcriptional repressor and the p38 MAP kinase: unlikely partners in G1 regulation and tumor suppression

被引:82
|
作者
Yee, AS
Paulson, EK
McDevitt, MA
Rieger-Christ, K
Summerhayese, I
Berasi, SP
Kim, J
Huang, CY
Zhang, XW
机构
[1] Tufts Univ, Sch Med, Dept Biochem, Boston, MA 02111 USA
[2] Tufts Univ, Sch Med, Genet Program, Boston, MA 02111 USA
[3] Tufts Univ New England Med Ctr, Dept Radiat Oncol, Boston, MA 02111 USA
[4] Johns Hopkins Univ, Sch Med, Div Hematol, Dept Med, Baltimore, MD 21205 USA
[5] RE Wise MD Res & Educ Inst, Lahey Clin, Cell & Mol Biol Lab, Burlington, MA 01805 USA
[6] Tufts Univ, Sch Nutr Sci & Policy, Program Cell & Mol Nutr, Boston, MA 02111 USA
关键词
HBP1; tumor suppressor; p38; MAPK; Wnt signaling; AXH; ataxin homology domain; HDAC; ROS; p47; phox; chromosome; 7;
D O I
10.1016/j.gene.2004.04.004
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Mechanisms that inhibit cell cycle progression and establish growth arrest are fundamental to tumor suppression and to normal cell differentiation. A complete understanding of these mechanisms should provide new diagnostic and therapeutic targets for future clinical applications related to cancer-specific pathways. This review will focus on the HMG-box protein 1 (HBP1) transcriptional repressor and its roles in cell cycle progression and tumor suppression. The work of several labs now suggests a new pathway for inhibiting G1 progression with exciting possible implications for tumor suppression. Our recent work suggests that the two previously unassociated proteins-the HBP1 transcription factor and the p38 MAP kinase pathway-may now participate together in a G1 regulatory network. Several recent papers collectively highlight an unexpected role and connection of the p38 MAP kinase-signaling pathway in cell cycle control, senescence, and tumor suppression. Together, these initially divergent observations may provide clues into a new tumor suppressive network and spur further investigations that may contribute to new diagnostic and therapeutic targets for cancer. (C) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:1 / 13
页数:13
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