Lack of imprinting of three human cyclin-dependent kinase inhibitor genes.
Genomic imprinting is an epigenetic modification in the germline leading to parental allele-specific gene expression in somatic cells. We have previously found that imprinted genes can be abnormally expressed or silenced in tumors and that the cyclin-dependent kinase inhibitor (CKI) CDKN1C (p57KIP2) is normally imprinted, with preferential expression of the maternal allele. Here we analyze the imprinting status of three additional CKIs, the abnormal expression and/or chromosomal localization of which has been implicated in human malignancy: CDKN1A, CDKN1B, and CDKN2C. Allele-specific expression was examined by reverse transcription-PCR, using primers that span transcribed polymorphisms as well as exon/intron boundaries, to distinguish cDNA products from genomic DNA. Biallelic expression was observed for all three genes in both fetal and adult tissues. Thus, genomic imprinting is not a generalized feature of CKIs.[1]References
- Lack of imprinting of three human cyclin-dependent kinase inhibitor genes. Cost, G.J., Thompson, J.S., Reichard, B.A., Lee, J.Y., Feinberg, A.P. Cancer Res. (1997) [Pubmed]
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