The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
mir-200c Regulates Induction of Apoptosis through CD95 by Targeting FAP-1
Open accessAbstract
SUMMARY Tumor progression shares many characteristics with the process of epithelial-to-mesenchymal transition (EMT). Cells that have undergone an EMT are known to have an increased resistance to apoptosis. CD95/Fas is an apoptosis-inducing receptor expressed on many tissues and tumor cells. During tumor progression CD95 is frequently downregulated, and tumor cells lose apoptosis sensitivity. miR-200 microRNAs repress both the EMT-inducing ZEB1 and ZEB2 transcription factors. We now demonstrate that miR-200c sensitizes cells to apoptosis mediated by CD95. We have identified the apoptosis inhibitor FAP-1 as a target for miR-200c. FAP-1 was demonstrated to be responsible for the reduced sensitivity to CD95-mediated apoptosis in cells with inhibited miR-200. The identification of FAP-1 as a miR-200c target provides a molecular mechanism to explain both the downregulation of CD95 expression and the reduction in sensitivity of cells to CD95-mediated apoptosis that is observed in the context of reduced miR-200 expression during tumor progression.
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Park, S.-M., Gaur, A. B., Lengyel, E., & Peter, M. E. (2008) · Genes & Development · doi:10.1101/gad.1640608 · Cited by 2,272
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Metadata
- Authors
- Schickel, R., Park, S.-M., Murmann, A. E., & Peter, M. E.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 38
- Issue
- 6
- Pages
- 908-915
- ISSN
- 1097-2765 (ISSN-L)
- OpenAlex
- W2099439420
- Cited by
- 167
- References
- 2
- FWCI
- 5.78
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Schickel, R., Park, S.-M., Murmann, A. E., & Peter, M. E. (2010). mir-200c Regulates Induction of Apoptosis through CD95 by Targeting FAP-1. Molecular Cell. https://doi.org/10.1016/j.molcel.2010.05.018
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