ALBERT — All Library Books, journals and Electronic Records Telegrafenberg

Unknown

Promotion of trophoblast stem cell proliferation by FGF4 (1998)

S. Tanaka ; T. Kunath ; A. K. Hadjantonakis ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 282(5396): 2072-5.

add to mindlist on the mindlist

Details

Publication Date: 1998-12-16

Description: The trophoblast cell lineage is essential for the survival of the mammalian embryo in utero. This lineage is specified before implantation into the uterus and is restricted to form the fetal portion of the placenta. A culture of mouse blastocysts or early postimplantation trophoblasts in the presence of fibroblast growth factor 4 (FGF4) permitted the isolation of permanent trophoblast stem cell lines. These cell lines differentiated to other trophoblast subtypes in vitro in the absence of FGF4 and exclusively contributed to the trophoblast lineage in vivo in chimeras.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, S -- Kunath, T -- Hadjantonakis, A K -- Nagy, A -- Rossant, J -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2072-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9851926" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Blastocyst/cytology ; Cell Differentiation ; Cell Division ; Cell Line ; Cell Lineage ; Chimera ; Culture Media, Conditioned ; Embryo, Mammalian/cytology ; Female ; Fibroblast Growth Factor 4 ; Fibroblast Growth Factors/*pharmacology/physiology ; Fibroblasts/cytology ; Gene Expression Regulation, Developmental ; Genetic Markers ; Karyotyping ; Male ; Mice ; Models, Biological ; Proto-Oncogene Proteins/*pharmacology/physiology ; Signal Transduction ; Stem Cells/*cytology/metabolism ; Trophoblasts/*cytology/metabolism

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

Permalink

	Location	Call Number	Expected	Availability

Others were also interested in ...

PAPER CURRENT

S·F·X

Fulltext

Unknown

Regulation of a transcription factor network required for differentiation and metabolism (1998)

S. A. Duncan ; M. A. Navas ; D. Dufort ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 281(5377): 692-5.

add to mindlist on the mindlist

Details

Publication Date: 1998-07-31

Description: Hepatocyte nuclear factors (HNFs) are a heterogeneous class of evolutionarily conserved transcription factors that are required for cellular differentiation and metabolism. Mutations in HNF-1alphaand HNF-4alpha genes impair insulin secretion and cause type 2 diabetes. Regulation of HNF-4/HNF-1 expression by HNF-3alpha and HNF-3beta was studied in embryoid bodies in which one or both HNF-3alpha or HNF-3beta alleles were inactivated. HNF-3beta positively regulated the expression of HNF-4alpha/HNF-1alpha and their downstream targets, implicating a role in diabetes. HNF-3beta was also necessary for expression of HNF-3alpha. In contrast, HNF-3alpha acts as a negative regulator of HNF-4alpha/HNF-1alpha demonstrating that HNF-3alpha and HNF-3beta have antagonistic transcriptional regulatory functions in vivo. HNF-3alpha does not appear to act as a classic biochemical repressor but rather exerts its negative effect by competing for HNF-3 binding sites with the more efficient activator HNF-3beta. In addition, the HNF-3alpha/HNF-3beta ratio is modulated by the presence of insulin, providing evidence that the HNF network may have important roles in mediating the action of insulin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duncan, S A -- Navas, M A -- Dufort, D -- Rossant, J -- Stoffel, M -- New York, N.Y. -- Science. 1998 Jul 31;281(5377):692-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratories of Molecular Cell Biology and Metabolic Diseases, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9685261" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Cell Differentiation ; Clone Cells ; DNA-Binding Proteins/genetics/*metabolism ; Diabetes Mellitus, Type 2/genetics/metabolism ; Embryonic and Fetal Development ; Endoderm/cytology/*metabolism ; *Gene Expression Regulation ; *Gene Expression Regulation, Developmental ; Gene Targeting ; Glucose/metabolism ; Hepatocyte Nuclear Factor 1 ; Hepatocyte Nuclear Factor 1-alpha ; Hepatocyte Nuclear Factor 1-beta ; Hepatocyte Nuclear Factor 3-alpha ; Hepatocyte Nuclear Factor 3-beta ; Hepatocyte Nuclear Factor 4 ; Insulin/pharmacology ; Mice ; Mutation ; Nuclear Proteins/genetics/*metabolism ; Phenotype ; Phosphoproteins/genetics ; Stem Cells ; Transcription Factors/genetics/*metabolism ; Up-Regulation

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

Permalink

	Location	Call Number	Expected	Availability

Others were also interested in ...

PAPER CURRENT

S·F·X

Fulltext

Unknown

Cardiac malformation in neonatal mice lacking connexin43 (1995)

A. G. Reaume ; P. A. de Sousa ; S. Kulkarni ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 267(5205): 1831-4.

add to mindlist on the mindlist

Details

Publication Date: 1995-03-24

Description: Gap junctions are made up of connexin proteins, which comprise a multigene family in mammals. Targeted mutagenesis of connexin43 (Cx43), one of the most prevalent connexin proteins, showed that its absence was compatible with survival of mouse embryos to term, even though mutant cell lines showed reduced dye coupling in vitro. However, mutant embryos died at birth, as a result of a failure in pulmonary gas exchange caused by a swelling and blockage of the right ventricular outflow tract from the heart. This finding suggests that Cx43 plays an essential role in heart development but that there is functional compensation among connexins in other parts of the developing fetus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reaume, A G -- de Sousa, P A -- Kulkarni, S -- Langille, B L -- Zhu, D -- Davies, T C -- Juneja, S C -- Kidder, G M -- Rossant, J -- New York, N.Y. -- Science. 1995 Mar 24;267(5205):1831-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7892609" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Cell Line ; Connexin 43/*genetics/*physiology ; Embryo, Mammalian/cytology ; Heart Defects, Congenital/*genetics/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Respiratory Transport/genetics ; Stem Cells ; Ventricular Outflow Obstruction/congenital/genetics

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics

Published by American Association for the Advancement of Science (AAAS)

Permalink