Linked Life Data

9876177

Source:http://linkedlifedata.com/resource/pubmed/id/9876177

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-3-4
pubmed:abstractText
Cripto-1(Cr1) protein encoded by the tdgf1 gene, is a secreted growth factor that is expressed early in embryonic development and is re-expressed in some tumors of the breast and colon. During embryonic development, Cr1 is expressed in inner cell mass cells and the primitive streak, and later is restricted to the developing heart. To investigate the role of Cr1 during mouse development, mice were generated that contain a null mutation of both Cr1 genes, derived from homologous recombination in embryonic stem cells. No homozygous Cr1-/- mice were born, indicating that Cr1 is necessary for embryonic development. Embryos initiated gastrulation and some embryos produced mesoderm up to day E7.5. Increasingly aberrant morphogenesis gave rise to disordered neuroepithelium that failed to produce a recognizable neural tube, or head-fold. Although some biochemical markers of differentiating ectoderm, mesoderm and endoderm were expressed, all the cardiac-specific markers were absent from day E8.7 embryos: (&agr;)MHC, betaMHC, MLC2A, MLC2V and ANF, whereas they were expressed in wild-type embryos. The yolk sac and placental tissues continued development in the absence of the embryo until day E9.5 but lacked large yolk sac blood vessels. Chimeric mice were constructed by microinjection of double targeted Cr1(-/- )embryonic stem cells into normal C57BL/6 blastocysts. The Cr1 produced by the normal C57BL/6 cells fully rescued the phenotype of Cr1(-/-) cells, indicating that Cr1 protein acted in a paracrine manner. Cells derived from the embryo proliferated and migrated poorly and had different adhesion properties compared to wild type. Therefore, lethality in the absence of Cr1, likely resulted largely from defective precardiac mesoderm that was unable to differentiate into functional cardiomyocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0950-1991
pubmed:author
pubmed:issnType
Print
pubmed:volume
126
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
483-94
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9876177-Alleles, pubmed-meshheading:9876177-Animals, pubmed-meshheading:9876177-Biological Markers, pubmed-meshheading:9876177-Cell Differentiation, pubmed-meshheading:9876177-Chimera, pubmed-meshheading:9876177-Culture Techniques, pubmed-meshheading:9876177-Epidermal Growth Factor, pubmed-meshheading:9876177-Fibroblasts, pubmed-meshheading:9876177-Gastrula, pubmed-meshheading:9876177-Genotype, pubmed-meshheading:9876177-Growth Substances, pubmed-meshheading:9876177-Heart, pubmed-meshheading:9876177-Homozygote, pubmed-meshheading:9876177-Membrane Glycoproteins, pubmed-meshheading:9876177-Mesoderm, pubmed-meshheading:9876177-Mice, pubmed-meshheading:9876177-Mice, Inbred C57BL, pubmed-meshheading:9876177-Morphogenesis, pubmed-meshheading:9876177-Myocardium, pubmed-meshheading:9876177-Neoplasm Proteins, pubmed-meshheading:9876177-Neovascularization, Physiologic, pubmed-meshheading:9876177-Phenotype
pubmed:year
1999
pubmed:articleTitle
Abrogation of the Cripto gene in mouse leads to failure of postgastrulation morphogenesis and lack of differentiation of cardiomyocytes.
pubmed:affiliation
The Burnham Institute, La Jolla Cancer Research Center, N. Torrey Pines Road, La Jolla, CA 92037, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't