Cited by 54Cancer-related Molecular PathwaysCell death mechanisms and regulationPI3K/AKT/mTOR signaling in cancer

CYFIP2, a Direct p53 Target, is Leptomycin-B Sensitive

Open access
Jackson II, Roger S., Cho, Yong-Jig, Stein, Susanne, Liang, Peng·2007·Cell Cycle

Abstract

A number of target genes for the tumor suppressor, p53, have been identified, however, the mechanisms that contribute to p53-dependent apoptosis remain to be fully elucidated. In a comprehensive screen for p53 target genes, we have identified Cytoplasmic FMR Interacting Protein 2 (CYFIP2) as a p53-inducible gene. Here we show that the CYFIP2 promoter contains a p53-responsive element that confers p53 binding as well as transcriptional activation of a heterologous reporter. Inducible expression of CYFIP2 is sufficient for caspase activation and cellular apoptosis, reminiscent of p53 activation. Together, these results suggest that CYFIP2 is a direct p53 target gene that may be part of a redundant network of genes responsible for p53-dependent apoptosis. In addition, the sensitivity of CYFIP2 protein subcellular localization to Leptomycin-B, a CRM-1/Exportin inhibitor, suggests that the biological functions of CYFIP2 may extend from the cytoplasmic compartment into the nucleus of the cell.

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  • Treatment of cells with leptomycin B (an inhibitor of the nuclear exporter CRM-1) induces the nuclear accumulation of ABI1 and CYFIP2.

    “Treatment of cells with leptomycin B (an inhibitor of the nuclear exporter CRM-1) induces the nuclear accumulation of ABI184 and CYFIP285.”

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Cited by

Sorted by citations

Authors
Jackson II, R. S., Cho, Y.-J., Stein, S., & Liang, P.
Affiliations
  • Vanderbilt-Ingram Cancer Center (US)
  • Johannes Gutenberg University Mainz (DE)
  • Vanderbilt University (US)
Venue
Cell Cycle
Published
2007-01
Volume
6
Issue
1
Pages
95-103
ISSN
  • 1538-4101 (ISSN-L)
  • 1551-4005
OpenAlex
W2030813056
Cited by
54
References
1
Citations by year
2026: 1 · 2025: 2 · 2024: 4 · 2023: 6 · 2022: 4 · 2021: 3 · 2020: 4 · 2019: 2 · 2018: 2 · 2017: 3 · 2015: 5 · 2014: 3 · 2013: 2 · 2012: 3
FWCI
1.27
Type
journal article
Language
en
Open access
Locations
  • Cell Cycle (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Vanderbilt University
  • National Institutes of Health
  • National Cancer Institute (CA76960, R01CA076960, R01CA105024, CA105024)
  • National Institute of General Medical Sciences (T32GM008554, GM08554-7)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords
CYFIP2, p53 target genes, p53 response elements, p53-dependent apoptosis, caspase activation, leptomycin B, nuclear export, protein localization, transcriptional activation
MeSH terms
Animals, Chlorocebus aethiops, Fatty Acids, Unsaturated, Humans, Subcellular Fractions, Transcriptional Activation, Tumor Suppressor Protein p53, Gene Targeting, COS Cells, Cell Line, Tumor, Adaptor Proteins, Signal Transducing

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