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

Amy S. Yee, Eric K. Paulson, Michael A. McDevitt, Kimberly Rieger-Christ, Ian Summerhayes, Stephen P. Berasi, Jiyoung Kim, Chun Yin Huang, Xiaowei Zhang

Research output: Contribution to journalReview articlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1-13
Number of pages13
JournalGene
Volume336
Issue number1
DOIs
StatePublished - Jul 7 2004

Keywords

  • AML
  • APC
  • AXH
  • Ataxin homology domain
  • Chromosome 7
  • GSK3β
  • HBP1
  • HDAC
  • HMG-box protein 1
  • ROS
  • Tumor suppressor
  • Wnt signaling
  • acute myelogenous leukemia
  • adenematous polypoisis coli
  • ataxin
  • glycogen synthase beta
  • p38 MAPK
  • p47 phox

ASJC Scopus subject areas

  • Genetics

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