CYFIP2, a Direct p53 Target, is Leptomycin-B Sensitive
Open accessAbstract
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.”
From The WAVE complex in developmental and adulthood brain disorders (2025) · cites this paper as [85]
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- 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)
- ORCID
- Liang, Peng
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- 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
- bronze
- doi.org
- 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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