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Enhanced CpG Mutability and Tumorigenesis in MBD4-Deficient Mice
Open accessAbstract
The mammalian protein MBD4 contains a methyl-CpG binding domain and can enzymatically remove thymine (T) or uracil (U) from a mismatched CpG site in vitro. These properties suggest that MBD4 might function in vivo to minimize the mutability of 5-methylcytosine by removing its deamination product from DNA. We tested this hypothesis by analyzing Mbd4 −/− mice and found that the frequency of of C → T transitions at CpG sites was increased by a factor of three. On a cancer-susceptible Apc Min/+ background, Mbd4 −/− mice showed accelerated tumor formation with CpG → TpG mutations in the Apc gene. Thus MBD4 suppresses CpG mutability and tumorigenesis in vivo.
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Citations
Cited by
Jaenisch, R., & Bird, A. (2003) · Nature Genetics · doi:10.1038/ng1089 · Cited by 6,325
Self-citationDNA methylation and its basic function
Moore, L. D., Le, T., & Fan, G. (2013) · Neuropsychopharmacology · doi:10.1038/npp.2012.112 · Cited by 4,906
Genomic DNA methylation: the mark and its mediators.
Klose, R. J., & Bird, A. P. (2006) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2005.12.008 · Cited by 2,501
Self-citationTargeting epigenetic regulators for cancer therapy: mechanisms and advances in clinical trials
Cheng, Y., He, C., Wang, M., Ma, X., Mo, F., Yang, S., Han, J., & Wei, X. (2019) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-019-0095-0 · Cited by 1,097
“Knockout of MBD4 indeed increased tumorigenesis in APC-background mice, which makes MBD4 a tumor suppressor.(68) MBD4 is important in DNA damage repair, given the interaction between MBD4 and MMR.”
BackgroundReversing DNA Methylation: Mechanisms, Genomics, and Biological Functions
Wu, H., & Zhang, Y. (2014) · Cell · doi:10.1016/j.cell.2013.12.019 · Cited by 1,065
“While other members of the UDG family of DNA glycosylases (UNG, MBD4, and SMUG1) are dispensable for embryonic development (Kemmerich et al., 2012; Millar et al., 2002), Tdg null mouse embryos exhibit a wide range of developmental defects and die around embryonic day (E) 12.5 (Cortázar et al.,…”
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Metadata
- Authors
- Millar, C. B., Guy, J., Sansom, O. J., Selfridge, J., MacDougall, E., Hendrich, B., Keightley, P. D., Bishop, S. M., Clarke, A. R., & Bird, A.
- Venue
- Science
- Published
- 2002-07-19
- Volume
- 297
- Issue
- 5580
- Pages
- 403-405
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2045749216
- Cited by
- 328
- References
- 0
- FWCI
- 6.16
- Type
- journal article
- Language
- en
- Open access
- green
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- Millar, C. B., Guy, J., Sansom, O. J., Selfridge, J., MacDougall, E., Hendrich, B., Keightley, P. D., Bishop, S. M., Clarke, A. R., & Bird, A. (2002). Enhanced CpG Mutability and Tumorigenesis in MBD4-Deficient Mice. Science. https://doi.org/10.1126/science.1073354
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