The HBP1 transcriptional repressor and the p38 MAP kinase: unlikely partners in G1 regulation and tumor suppression
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-sp...
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Published in: | Gene Vol. 336; no. 1; pp. 1 - 13 |
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Main Authors: | , , , , , , , , |
Format: | Book Review Journal Article |
Language: | English |
Published: |
Netherlands
Elsevier B.V
07-07-2004
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Subjects: | |
Online Access: | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-3 ObjectType-Review-2 |
ISSN: | 0378-1119 1879-0038 |
DOI: | 10.1016/j.gene.2004.04.004 |