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

共 99 条

[51] Genome-wide scan of bipolar disorder in 65 pedigrees: supportative evidence for linkage at 8q24, 18q22, 4q32, 2p12, and 13q12 [J].

McInnis, MG ;

Lan, TH ;

Willour, VL ;

McMahon, FJ ;

Simpson, SG ;

Addington, AM ;

MacKinnon, DF ;

Potash, JB ;

Mahony, AT ;

Chellis, J ;

Huo, Y ;

Swift-Scanlan, T ;

Chen, H ;

Koskela, R ;

Stine, OC ;

Jamison, KR ;

Holmans, P ;

Folstein, SE ;

Ranade, K ;

Friddle, C ;

Botstein, D ;

Marr, T ;

Beaty, TH ;

Zandi, P ;

DePaulo, JR .

MOLECULAR PSYCHIATRY, 2003, 8 (03) :288-298

[52] Developmental origins of the metabolic syndrome: Prediction, plasticity, and programming [J].

McMillen, IC ;

Robinson, JS .

PHYSIOLOGICAL REVIEWS, 2005, 85 (02) :571-633

[53] The two-pore domain potassium channel TASK3 functionally impacts glioma cell death [J].

Meuth, Sven G. ;

Herrmann, Alexander M. ;

Ip, Chi W. ;

Kanyshkova, Tatyana ;

Bittner, Stefan ;

Weishaupt, Andreas ;

Budde, Thomas ;

Wiendl, Heinz .

JOURNAL OF NEURO-ONCOLOGY, 2008, 87 (03) :263-270

[54] GENOMIC IMPRINTING IN MAMMALIAN DEVELOPMENT - A PARENTAL TUG-OF-WAR [J].

MOORE, T ;

HAIG, D .

TRENDS IN GENETICS, 1991, 7 (02) :45-49

[55]

Morgan DK, 2009, NESTLE NUTR WORKS SE, V63, P109, DOI 10.1159/000209976

[56] A census of mammalian imprinting [J].

Morison, IM ;

Ramsay, JP ;

Spencer, HG .

TRENDS IN GENETICS, 2005, 21 (08) :457-465

[57] Genomic amplification and oncogenic properties of the KCNK9 potassium channel gene [J].

Mu, D ;

Chen, LY ;

Zhang, XP ;

See, LH ;

Koch, CM ;

Yen, C ;

Tong, JJ ;

Spiegel, L ;

Nguyen, KCQ ;

Servoss, A ;

Peng, Y ;

Pei, L ;

Marks, JR ;

Lowe, S ;

Hoey, T ;

Jan, LY ;

McCombie, WR ;

Wigler, MH ;

Powers, S .

CANCER CELL, 2003, 3 (03) :297-302

[58] The monogenic primary dystonias [J].

Mueller, Ulrich .

BRAIN, 2009, 132 :2005-2025

[59] Imprinting evolution and the price of silence [J].

Murphy, SK ;

Jirtle, RL .

BIOESSAYS, 2003, 25 (06) :577-588

[60] Epigenetics and assisted reproductive technology: A call for investigation [J].

Niemitz, EL ;

Feinberg, AP .

AMERICAN JOURNAL OF HUMAN GENETICS, 2004, 74 (04) :599-609

← 1 2 3 4 5 6 7 8 9 10 →