Literature DB >> 15108320

Different molecular mechanisms underlie placental overgrowth phenotypes caused by interspecies hybridization, cloning, and Esx1 mutation.

Umashankar Singh1, Laurel E Fohn, Teruhiko Wakayama, Jun Ohgane, Christine Steinhoff, Bettina Lipkowitz, Ralph Schulz, Annie Orth, H Hilger Ropers, Richard R Behringer, Satoshi Tanaka, Kunio Shiota, Ryuzo Yanagimachi, Ulrike A Nuber, Reinald Fundele.   

Abstract

To obtain a deeper insight into the genes and gene networks involved in the development of placentopathies, we have assessed global gene expression in three different models of placental hyperplasia caused by interspecies hybridization (IHPD), cloning by nuclear transfer, and mutation of the Esx1 gene, respectively. Comparison of gene expression profiles of approximately 13,000 expressed sequence tags (ESTs) identified specific subsets of genes with changed expression levels in IHPD, cloned, and Esx1 mutant placentas. Of interest, only one gene of known function and one EST of unknown function were found common to all three placentopathies; however, a significant number of ESTs were common to IHPD and cloned placentas. In contrast, only one gene was shared between IHPD and Esx1 mutant, and cloned and Esx1 mutant placentas, respectively. These genes common to different abnormal placental growth genotypes are likely to be important in the occurrence of placentopathy. Copyright 2004 Wiley-Liss, Inc.

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Year:  2004        PMID: 15108320     DOI: 10.1002/dvdy.20024

Source DB:  PubMed          Journal:  Dev Dyn        ISSN: 1058-8388            Impact factor:   3.780


  10 in total

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Review 6.  Epigenetic aberrations and cancer.

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9.  Somatic donor cell type correlates with embryonic, but not extra-embryonic, gene expression in postimplantation cloned embryos.

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10.  Expression of Human Placenta-specific 1 (PLAC1) in CHO-K1 Cells.

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  10 in total

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