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Mediation of the DCC Apoptotic Signal by DIP13α
Open accessAbstract
DCC (deleted in colorectal cancer) is a candidate tumor suppressor gene. However the function of DCC remains elusive. Previously, we demonstrated that forced expression of DCC induces apoptosis or cell cycle arrest (Chen, Y. Q., Hsieh, J. T., Yao, F., Fang, B., Pong, R. C., Cipriano, S. C. & Krepulat, F. (1999) Oncogene 18, 2747-2754). To delineate the DCC-induced apoptotic pathway, we have identified a protein, DIP13 alpha, which interacts with DCC. The DIP13 alpha protein has a pleckstrin homology domain and a phosphotyrosine binding domain. It interacts with a region on the DCC cytoplasmic domain that is required for the induction of apoptosis. Although ectopic expression of DIP13 alpha alone causes only a slight increase in apoptosis, co-expression of DCC and DIP13 alpha results in an approximately 5-fold increase in apoptosis. Removal of the DCC-interacting domain on DIP13 alpha abolishes its ability to enhance DCC-induced apoptosis. Inhibition of endogenous DIP13 alpha expression by small interfering RNA blocks DCC-induced apoptosis. Our data suggest that DIP13 alpha is a mediator of the DCC apoptotic pathway.
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“(1) DCC is cleaved by CASP3 and this promotes its association with adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper 1 (APPL1) and CASP9, resulting in the activation of the CASP9-CASP3 cascade [350, 351]”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [351]
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Metadata
- Authors
- Liu, J., Yao, F., Wu, R., Morgan, M., Thorburn, A., Finley, R. L., & Chen, Y. Q.
- Affiliations
- Wayne State University (US)
- Wake Forest University Health Sciences (US)
- Corresponding author
- Chen, Yong Q.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2002-07
- Volume
- 277
- Issue
- 29
- Pages
- 26281-26285
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2046818223
- Cited by
- 120
- References
- 25
- Citations by year
- 2025: 2 · 2023: 2 · 2022: 3 · 2021: 1 · 2020: 4 · 2019: 1 · 2018: 7 · 2017: 6 · 2016: 7 · 2015: 1 · 2014: 1 · 2013: 2 · 2012: 8
- FWCI
- 4.86
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ca077489-06)
- National Cancer Institute (R01CA77489)
- 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 › Protein Kinase Regulation and GTPase Signaling
- Keywords
- DCC, apoptosis, tumor suppressor, protein-protein interaction, pleckstrin homology domain, phosphotyrosine binding domain, cytoplasmic domain, cell cycle arrest, siRNA knockdown
- MeSH terms
- Animals, Carrier Proteins, Molecular Sequence Data, Peptide Mapping, Rabbits, Tumor Cells, Cultured, Yeasts, Colorectal Neoplasms, Genes, DCC, Apoptosis, Phosphotyrosine, RNA, Untranslated, RNA, Small Interfering, Adaptor Proteins, Signal Transducing
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