The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
PERP, an apoptosis-associated target of p53, is a novel member of the PMP-22/gas3 family
Open accessAbstract
The p53 tumor suppressor activates either cell cycle arrest or apoptosis in response to cellular stress. Mouse embryo fibroblasts (MEFs) provide a powerful primary cell system to study both p53-dependent pathways. Specifically, in response to DNA damage, MEFs undergo p53-dependent G 1 arrest, whereas MEFs expressing the adenovirus E1A oncoprotein undergo p53-dependent apoptosis. As the p53-dependent apoptosis pathway is not well understood, we sought to identify apoptosis-specific p53 target genes using a subtractive cloning strategy. Here, we describe the characterization of a gene identified in this screen, PERP, which is expressed in a p53-dependent manner and at high levels in apoptotic cells compared with G 1-arrested cells. PERP induction is linked to p53-dependent apoptosis, including in response to E2F-1-driven hyperproliferation. Furthermore, analysis of the PERP promoter suggests that PERP is directly activated by p53. PERP shows sequence similarity to the PMP-22/gas3 tetraspan membrane protein implicated in hereditary human neuropathies such as Charcot–Marie–Tooth. Like PMP-22/gas3, PERP is a plasma membrane protein, and importantly, its expression causes cell death in fibroblasts. Taken together, these data suggest that PERP is a novel effector of p53-dependent apoptosis.
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Cites
Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
Oltval, Z. N., Milliman, C. L., & Korsmeyer, S. J. (1993) · Cell · doi:10.1016/0092-8674(93)90509-o · Cited by 6,003
Kastan, M. B., Zhan, Q., El-Deiry, W. S., Carrier, F., Jacks, T., Walsh, W. V., Plunkett, B. S., Vogelstein, B., & Fornace, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90593-2 · Cited by 3,047
Self-citationHypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours
Graeber, T. G., Osmanian, C., Jacks, T., Housman, D. E., Koch, C. J., Lowe, S. W., & Giaccia, A. J. (1996) · Nature · doi:10.1038/379088a0 · Cited by 2,300
Self-citationMice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control
Deng, C., Zhang, P., Wade Harper, J., Elledge, S. J., & Leder, P. (1995) · Cell · doi:10.1016/0092-8674(95)90039-x · Cited by 2,113
Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization
Zindy, F., Eischen, C. M., Randle, D. H., Kamijo, T., Cleveland, J. L., Sherr, C. J., & Roussel, M. F. (1998) · Genes & Development · doi:10.1101/gad.12.15.2424 · Cited by 1,245
Radiation-induced cell cycle arrest compromised by p21 deficiency
Brugarolas, J., Chandrasekaran, C., Gordon, J. I., Beach, D., Jacks, T., & Hannon, G. J. (1995) · Nature · doi:10.1038/377552a0 · Cited by 1,242 · cited 1×
“Dishes of both treated and untreated wild-type and p53−/− MEFs were collected after 18 hr of doxorubicin treatment for FACS analysis to verify a p53-dependent G1 arrest, as described previously (Brugarolas et al. 1995).”
MethodSelf-citationp53-Dependent apoptosis suppresses tumor growth and progression in vivo
Symonds, H., Krall, L., Remington, L., Saenz-Robles, M., Lowe, S., Jacks, T., & Van Dyke, T. (1994) · Cell · doi:10.1016/0092-8674(94)90534-7 · Cited by 880
Self-citationCyclin G is a transcriptional target of the p53 tumor suppressor protein.
Okamoto, K., & Beach, D. (1994) · The EMBO Journal · doi:10.1002/j.1460-2075.1994.tb06807.x · Cited by 455
Hurford, R. K., Cobrinik, D., Lee, M. H., & Dyson, N. (1997) · Genes & Development · doi:10.1101/gad.11.11.1447 · Cited by 431
Cited by
Fridman, J. S., & Lowe, S. W. (2003) · Oncogene · doi:10.1038/sj.onc.1207116 · Cited by 1,401
Self-citationHaupt, S., Berger, M., Goldberg, Z., & Haupt, Y. (2003) · Journal of Cell Science · doi:10.1242/jcs.00739 · Cited by 1,136
Defying death after DNA damage
Rich, T., Allen, R. L., & Wyllie, A. H. (2000) · Nature · doi:10.1038/35037717 · Cited by 724
Regulation and function of the p53 tumor suppressor protein
Ryan, K. M., Phillips, A. C., & Vousden, K. H. (2001) · Current Opinion in Cell Biology · doi:10.1016/s0955-0674(00)00216-7 · Cited by 721
Barlev, N. A., Liu, L., Chehab, N. H., Mansfield, K., Harris, K. G., Halazonetis, T. D., & Berger, S. L. (2001) · Molecular Cell · doi:10.1016/s1097-2765(01)00414-2 · Cited by 710
Metadata
- Authors
- Attardi, L. D., Reczek, E. E., Cosmas, C., Demicco, E. G., McCurrach, M. E., Lowe, S. W., & Jacks, T.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2000-03-15
- Volume
- 14
- Issue
- 6
- Pages
- 704-718
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2155363874
- Cited by
- 397
- References
- 9
- Type
- posted content
- Language
- en
- Open access
- diamond
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- Attardi, L. D., Reczek, E. E., Cosmas, C., Demicco, E. G., McCurrach, M. E., Lowe, S. W., & Jacks, T. (2000). PERP, an apoptosis-associated target of p53, is a novel member of the PMP-22/gas3 family. Genes & Development. https://doi.org/10.1101/gad.14.6.704
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