Different molecular mechanisms underlie placental overgrowth phenotypes caused by interspecies hybridization, cloning, and Esx1 mutation
(2004) In Developmental Dynamics 230(1). p.149-164- 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... (More)
- 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. (Less)
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https://lup.lub.lu.se/record/1131039
- author
- publishing date
- 2004
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Developmental Dynamics
- volume
- 230
- issue
- 1
- pages
- 149 - 164
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- pmid:15108320
- scopus:11144354460
- ISSN
- 1097-0177
- DOI
- 10.1002/dvdy.20024
- language
- English
- LU publication?
- no
- id
- 42eb01a3-b542-4337-b7a3-85d01df5db74 (old id 1131039)
- date added to LUP
- 2016-04-01 12:37:28
- date last changed
- 2022-01-27 07:39:23
@article{42eb01a3-b542-4337-b7a3-85d01df5db74, 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.}}, author = {{Singh, Umashankar and Fohn, Laurel E and Wakayama, Teruhiko and Ohgane, Jun and Steinhoff, Christine and Lipkowitz, Bettina and Schulz, Ralph and Orth, Annie and Ropers, H Hilger and Behringer, Richard R and Tanaka, Satoshi and Shiota, Kunio and Yanagimachi, Ryuzo and Nuber, Ulrike}}, issn = {{1097-0177}}, language = {{eng}}, number = {{1}}, pages = {{149--164}}, publisher = {{John Wiley & Sons Inc.}}, series = {{Developmental Dynamics}}, title = {{Different molecular mechanisms underlie placental overgrowth phenotypes caused by interspecies hybridization, cloning, and Esx1 mutation}}, url = {{http://dx.doi.org/10.1002/dvdy.20024}}, doi = {{10.1002/dvdy.20024}}, volume = {{230}}, year = {{2004}}, }