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- Publisher Website: 10.1101/gad.12.1.107
- Scopus: eid_2-s2.0-15444348295
- PMID: 9420335
- WOS: WOS:000071455400011
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Article: The tumor suppressor gene Smad4/Dpc4 is required for gastrulation and later for anterior development of the mouse embryo
Title | The tumor suppressor gene Smad4/Dpc4 is required for gastrulation and later for anterior development of the mouse embryo |
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Authors | |
Keywords | Visceral endoderm Anterior development Gastrulation Smad4/Dpc4 mutant mice |
Issue Date | 1998 |
Citation | Genes and Development, 1998, v. 12, n. 1, p. 107-119 How to Cite? |
Abstract | Mutations in the SMAD4/DPC4 tumor suppressor gene, a key signal transducer in most TGFβ-related pathways, are involved in 50% of pancreatic cancers. Homozygous Smad4 mutant mice die before day 7.5 of embryogenesis. Mutant embryos have reduced size, fail to gastrulate or express a mesodermal marker, and show abnormal visceral endoderm development. Growth retardation of the Smad4-deficient embryos results from reduced cell proliferation rather than increased apoptosis. Aggregation of mutant Smad4 ES cells with wild- type tetraploid morulae rescues the gastrulation defect. These results indicate that Smad4 is initially required for the differentiation of the visceral endoderm and that the gastrulation defect in the epiblast is secondary and non-cell autonomous. Rescued embryos show severe anterior truncations, indicating a second important role for Smad4 in anterior patterning during embryogenesis. |
Persistent Identifier | http://hdl.handle.net/10722/291698 |
ISSN | 2023 Impact Factor: 7.5 2023 SCImago Journal Rankings: 5.015 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Sirard, Christian | - |
dc.contributor.author | De La Pompa, José Luis | - |
dc.contributor.author | Elia, Andrew | - |
dc.contributor.author | Itie, Annick | - |
dc.contributor.author | Mirtsos, Christine | - |
dc.contributor.author | Cheung, Alison | - |
dc.contributor.author | Hahn, Stephan | - |
dc.contributor.author | Wakeham, Andrew | - |
dc.contributor.author | Schwartz, Lois | - |
dc.contributor.author | Kern, Scott E. | - |
dc.contributor.author | Rossant, Janet | - |
dc.contributor.author | Mak, Tak W. | - |
dc.date.accessioned | 2020-11-17T14:54:55Z | - |
dc.date.available | 2020-11-17T14:54:55Z | - |
dc.date.issued | 1998 | - |
dc.identifier.citation | Genes and Development, 1998, v. 12, n. 1, p. 107-119 | - |
dc.identifier.issn | 0890-9369 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291698 | - |
dc.description.abstract | Mutations in the SMAD4/DPC4 tumor suppressor gene, a key signal transducer in most TGFβ-related pathways, are involved in 50% of pancreatic cancers. Homozygous Smad4 mutant mice die before day 7.5 of embryogenesis. Mutant embryos have reduced size, fail to gastrulate or express a mesodermal marker, and show abnormal visceral endoderm development. Growth retardation of the Smad4-deficient embryos results from reduced cell proliferation rather than increased apoptosis. Aggregation of mutant Smad4 ES cells with wild- type tetraploid morulae rescues the gastrulation defect. These results indicate that Smad4 is initially required for the differentiation of the visceral endoderm and that the gastrulation defect in the epiblast is secondary and non-cell autonomous. Rescued embryos show severe anterior truncations, indicating a second important role for Smad4 in anterior patterning during embryogenesis. | - |
dc.language | eng | - |
dc.relation.ispartof | Genes and Development | - |
dc.subject | Visceral endoderm | - |
dc.subject | Anterior development | - |
dc.subject | Gastrulation | - |
dc.subject | Smad4/Dpc4 mutant mice | - |
dc.title | The tumor suppressor gene Smad4/Dpc4 is required for gastrulation and later for anterior development of the mouse embryo | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1101/gad.12.1.107 | - |
dc.identifier.pmid | 9420335 | - |
dc.identifier.pmcid | PMC316400 | - |
dc.identifier.scopus | eid_2-s2.0-15444348295 | - |
dc.identifier.volume | 12 | - |
dc.identifier.issue | 1 | - |
dc.identifier.spage | 107 | - |
dc.identifier.epage | 119 | - |
dc.identifier.isi | WOS:000071455400011 | - |
dc.identifier.issnl | 0890-9369 | - |