Imprinting evolution and human health

被引：60

作者：

Das, Radhika ^{[2
,3
]}

Hampton, Daniel D. ^{[4
]}

Jirtle, Randy L. ^{[1
,3
]}

机构：

[1] Duke Univ, Med Ctr, Dept Radiat Oncol, Durham, NC 27710 USA

[2] Duke Univ, Med Ctr, Dept Radiat Oncol, Durham, NC 27710 USA

[3] Duke Univ, Med Ctr, Univ Program Genet & Genom, Durham, NC 27710 USA

[4] Duke Univ, Med Ctr, Dept Gastroenterol, Durham, NC 27710 USA

来源：

MAMMALIAN GENOME | 2009年 / 20卷 / 9-10期

关键词：

COMPARATIVE PHYLOGENETIC ANALYSIS; DIFFERENTIAL METHYLATION; PRENATAL EXPOSURE; DNA METHYLATION; MOUSE; GENE; EPIGENETICS; IGF2; EXPRESSION; SCHIZOPHRENIA;

D O I：

10.1007/s00335-009-9229-y

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Genomic imprinting results in parent-of-origin-dependent, monoallelic expression of genes. The functional haploid state of these genes has far-reaching consequences. Not only has imprinting been implicated in accelerating mammalian speciation, there is growing evidence that it is also involved in the pathogenesis of several human conditions, particularly cancer and neurological disorders. Epigenetic regulatory mechanisms govern the parental allele-specific silencing of imprinted genes, and many theories have attempted to explain the driving force for the evolution of this unique form of gene control. This review discusses the evolution of imprinting in Therian mammals, and the importance of imprinted genes in human health and disease.

引用

页码：563 / 572

页数：10

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