Regular ArticleMaternal and Paternal Chromosomes 7 Show Differential Methylation of Many Genes in Lymphoblast DNA
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Abnormal villous morphology associated with triple trisomy of paternal origin
2010, Journal of Molecular DiagnosticsCitation Excerpt :Since maternally derived (digynic) triploidy is not associated with molar-type morphological alterations of the villi, it is possible that an imbalance of imprinted gene expression is responsible for the villous changes in PHMs. Both chromosomes 7 and 20 contain significant regions of imprinting, which may have contributed to altered gene expression and possibly to the morphological alterations suggestive of a PHM in this case.33,34 It is possible that both the specific chromosomes involved and the dosage (number) of extra paternal chromosomes may act in concert to influence villous morphology since one study found that the parental origin of trisomy for only chromosome 7 did not affect the placental morphology.35
Private inherited microdeletion/microduplications: Implications in clinical practice
2008, European Journal of Medical GeneticsCitation Excerpt :Four rearrangements are inherited from the mother and six from the father. Although none of the rearrangements contains proved imprinted genes, some of them are on chromosomes in which maternal or paternal imprinting has been reported such as chromosome 7 or 14 [6,13]. Six out of 10 rearrangements (0.4–1.6 Mb) cover entirely not polymorphic regions.
DLX5 and DLX6 expression is biallelic and not modulated by MeCP2 deficiency
2007, American Journal of Human GeneticsCitation Excerpt :Allelic variation in gene expression for nonimprinted genes is increasingly being recognized. The magnitude varies from a 1.3-fold to 9-fold difference in 20%–50% of the genes tested.62–66 Interestingly, allelic transcript variants may follow Mendelian inheritance because of variation in cis-acting elements or “regulatory SNPs.”67
Association of specific language impairment (SLI) to the region of 7q31
2003, American Journal of Human GeneticsAnalysis of GNAS1 and overlapping transcripts identifies the parental origin of mutations in patients with sporadic Albright hereditary osteodystrophy and reveals a model system in which to observe the effects of splicing mutations on translated and untranslated messenger RNA
2003, American Journal of Human GeneticsCitation Excerpt :Imprinting of NESP55 and XLαs has been demonstrated in a range of human fetal tissues (Hayward et al. 1998; Hayward and Bonthron 2000), and paternal expression of exon 1A has been demonstrated in cDNA extracted from whole blood (Liu et al. 2000). However, skewed imprinting and loss of imprinting in lymphoblasts have occasionally been reported (Antequera et al. 1990; Kubota et al. 1996; Hannula et al. 2001). For that reason, we tested whether imprinting of NESP55 and exon 1A was conserved in lymphoblastoid cell lines.
Utility of Lymphoblastoid Cell Lines for Induced Pluripotent Stem Cell Generation
2016, Stem Cells International
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