http://www.cnr.it/ontology/cnr/individuo/prodotto/ID168798
Modulation of angiogenesis by a tetrameric tripeptide that antagonizes vascular endothelial growth factor receptor 1 (Articolo in rivista)
- Type
- Label
- Modulation of angiogenesis by a tetrameric tripeptide that antagonizes vascular endothelial growth factor receptor 1 (Articolo in rivista) (literal)
- Anno
- 2008-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1074/jbc.M806607200 (literal)
- Alternative label
Ponticelli S.; Marasco D.; Tarallo V.; Albuquerque R.J.; Mitola S.; Takeda A.; Stassen J.M.; Presta M.; Ambati J.; Ruvo M.; De Falco S. (2008)
Modulation of angiogenesis by a tetrameric tripeptide that antagonizes vascular endothelial growth factor receptor 1
in The Journal of biological chemistry (Print); American Society Of Biochemistry And Molecular Biology Inc. (ASBMB), Rockville (Stati Uniti d'America)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Ponticelli S.; Marasco D.; Tarallo V.; Albuquerque R.J.; Mitola S.; Takeda A.; Stassen J.M.; Presta M.; Ambati J.; Ruvo M.; De Falco S. (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
- http://www.jbc.org/content/283/49/34250.long (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#descrizioneSinteticaDelProdotto
- Pubblicazione su rivista internazionale (literal)
- Note
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Angiogenesis Laboratory and Stem Cell Fate Laboratory, Institute of Genetics and Biophysics Adriano
Buzzati-Traverso, Consiglio Nazionale delle Ricerche (CNR), 80131 Napoli, Italy,
Institute of Biostructures and Bioimaging, CNR, 80134 Napoli, Italy
Department of Ophthalmology and Visual Sciences, University of Kentucky,
Lexington, Kentucky 40536,
Unit of General Pathology and Immunology, Department of Biomedical Sciences and Biotechnology,
University of Brescia, 25123 Brescia, Italy,
Thrombogenics, Campus Gasthuisberg, B-3000 Leuven, Belgium (literal)
- Titolo
- Modulation of angiogenesis by a tetrameric tripeptide that antagonizes vascular endothelial growth factor receptor 1 (literal)
- Abstract
- Vascular endothelial growth factor receptor-1 (VEGFR-1, also
known as Flt-1) is involved in complex biological processes often
associated to severe pathological conditions like cancer, inflammation,
andmetastasis formation. Consequently, the search for antagonists
of Flt-1 has recently gained a growing interest. Here we
report the identification of a tetrameric tripeptide from a combinatorial
peptide library built using non-natural amino acids, which
binds Flt-1 and inhibits in vitro its interaction with placental
growth factor (PlGF) and vascular endothelial growth factor
(VEGF) A and B (IC50=10µM). The peptide is stable in serum for
7 days and prevents both Flt-1 phosphorylation and the capillarylike
tube formation of human primary endothelial cells stimulated
by PlGF or VEGF-A. Conversely, the identified peptide does not
interfere in VEGF-induced VEGFR-2 activation. In vivo, this peptide
inhibits VEGF-A- and PlGF-induced neoangiogenesis in the
chicken embryo chorioallantoic membrane assay. In contrast, in
the cornea, where avascularity is maintained by high levels of
expression of the soluble form of Flt-1 receptor (sFlt-1) that prevents
the VEGF-A activity, the peptide is able to stimulate corneal
mouse neovascularization in physiological condition, as reported
previously for others neutralizing anti-Flt-1 molecules. This tetrameric
tripeptide represents a new, promising compound for
therapeutic approaches in pathologies where Flt-1 activation plays
a crucial role. (literal)
- Editore
- Prodotto di
- Autore CNR
- Insieme di parole chiave
Incoming links:
- Prodotto
- Autore CNR di
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi
- Editore di
- Insieme di parole chiave di