http://www.cnr.it/ontology/cnr/individuo/prodotto/ID59289
SIP-1 and MiRna 200 Family Define a Nitric Oxide-Dependent Molecular Circuitry Involved in Embryonic Stem Cells Vascular Differentiation (Articolo in rivista)
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- Label
- SIP-1 and MiRna 200 Family Define a Nitric Oxide-Dependent Molecular Circuitry Involved in Embryonic Stem Cells Vascular Differentiation (Articolo in rivista) (literal)
- Anno
- 2011-01-01T00:00:00+01:00 (literal)
- Alternative label
Rosati J., Spallotta F., Grasselli A., Antonini A., Vincentie S., Presutti C, Nanni S., Farsetti A., Capogrossi M.C., Illi B., Gaetano C. (2011)
SIP-1 and MiRna 200 Family Define a Nitric Oxide-Dependent Molecular Circuitry Involved in Embryonic Stem Cells Vascular Differentiation
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Rosati J., Spallotta F., Grasselli A., Antonini A., Vincentie S., Presutti C, Nanni S., Farsetti A., Capogrossi M.C., Illi B., Gaetano C. (literal)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#altreInformazioni
- Epub 2011 Jan 13. (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
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- ISI Web of Science (WOS) (literal)
- Titolo
- SIP-1 and MiRna 200 Family Define a Nitric Oxide-Dependent Molecular Circuitry Involved in Embryonic Stem Cells Vascular Differentiation (literal)
- Abstract
- OBJECTIVE: Smad-interacting protein-1 (Sip1/ZEB2) is a transcriptional repressor of the telomerase reverse transcriptase catalytic subunit (Tert) and has recently been identified as a key regulator of embryonic cell fate with a phenotypic effect similar, in our opinion, to that reported for nitric oxide (NO). Remarkably, SIP1/ZEB2 is a known target of the microRNA 200 (miR-200) family. In this light, we postulated that Sip1/ZEB2 and the miR-200 family could play a role during the NO-dependent differentiation of mES.
METHODS AND RESULTS: The results of the present study show that Sip1/ZEB2 expression is downregulated during the NO-dependent expression of mesendoderm and early cardiovascular precursor markers, including Flk1 and CXCR4 in mES. Coincidently, members of the miR-200 family, namely miR-429, -200a, -200b, and -200c, were transcriptionally induced in parallel to mouse Tert. This regulation occurred at the level of chromatin. Remarkably, miR-429/miR-200a overexpression or Sip1/ZEB2 knockdown by short hairpin RNA interference elicited a gene expression pattern similar to that of NO regardless of the presence of leukemia inhibitory factor.
CONCLUSIONS: These results are the first demonstrating that the miR-200 family and Sip1/ZEB2 transcription factor are regulated by NO, indicating an unprecedented molecular circuitry important for telomerase regulation and early differentiation of mES.
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