Modulation of imprinted gene network in placenta results in normal development of in vitro manipulated mouse embryos. (Q54441687)

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18 January 2020

title

Modulation of imprinted gene network in placenta results in normal development of in vitro manipulated mouse embryos (English)

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18 January 2020

3

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18 January 2020

Laurent Journot

4

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18 January 2020

Anne Gabory

5

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18 January 2020

author name string

Patricia Fauque

1

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18 January 2020

Marie-Anne Ripoche

2

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18 January 2020

Florence Busato

6

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18 January 2020

Anne Le Digarcher

7

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18 January 2020

Françoise Mondon

8

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18 January 2020

Ivo Gut

9

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18 January 2020

Pierre Jouannet

10

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18 January 2020

Daniel Vaiman

11

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18 January 2020

Luisa Dandolo

12

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18 January 2020

Hélène Jammes

13

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18 January 2020

publication date

11 February 2010

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18 January 2020

published in

Human Molecular Genetics

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18 January 2020

volume

19

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18 January 2020

page(s)

1779-1790

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18 January 2020

issue

9

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Assisted reproductive technology in Europe, 2004: results generated from European registers by ESHRE.

18 January 2020

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Silver-Russell syndrome in a girl born after in vitro fertilization: partial hypermethylation at the differentially methylated region of PEG1/MEST

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Assisted Reproductive Technology affects developmental kinetics, H19 Imprinting Control Region methylation and H19 gene expression in individual mouse embryos

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Zac1 regulates an imprinted gene network critically involved in the control of embryonic growth

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Mouse mutant embryos overexpressing IGF-II exhibit phenotypic features of the Beckwith-Wiedemann and Simpson-Golabi-Behmel syndromes

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Regulation of supply and demand for maternal nutrients in mammals by imprinted genes.

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IVF results in de novo DNA methylation and histone methylation at an Igf2-H19 imprinting epigenetic switch

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Epigenetic modifications in an imprinting cluster are controlled by a hierarchy of DMRs suggesting long-range chromatin interactions.

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Imprinting along the Kcnq1 domain on mouse chromosome 7 involves repressive histone methylation and recruitment of Polycomb group complexes.

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