http://www.cnr.it/ontology/cnr/individuo/prodotto/ID26658
Identification of placenta growth factor determinants for binding and activation of Flt-1 receptor (Articolo in rivista)
- Type
- Label
- Identification of placenta growth factor determinants for binding and activation of Flt-1 receptor (Articolo in rivista) (literal)
- Anno
- 2004-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1074/jbc.M401418200 (literal)
- Alternative label
Errico M.; Riccioni T.; Iyer S.; Pisano C.; Acharya K.R.; Persico M.G.; De Falco S. (2004)
Identification of placenta growth factor determinants for binding and activation of Flt-1 receptor
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
- Errico M.; Riccioni T.; Iyer S.; Pisano C.; Acharya K.R.; Persico M.G.; De Falco S. (literal)
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- Pagina fine
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- http://www.jbc.org/content/279/42/43929.long (literal)
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- Note
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- CNR, Inst Genet & Biophys Adriano Buzzati Traverso, I-80131 Naples, Italy; Sigma Tau Pharmaceut Co, Ind Farmaceut Riunite, Res & Dev, I-00040 Pomezia, Rome, Italy; Univ Bath, Dept Biol & Biochem, Bath BA2 7AY, Avon, England. (literal)
- Titolo
- Identification of placenta growth factor determinants for binding and activation of Flt-1 receptor (literal)
- Abstract
- Placenta growth factor (PlGF) belongs to the vascular
endothelial growth factor (VEGF) family and represents
a key regulator of angiogenic events in pathological conditions.
PlGF exerts its biological function through the
binding and activation of the seven immunoglobulinlike
domain receptor Flt-1, also known as VEGFR-1.
Here, we report the first detailed mutagenesis studies
that provide a basis for understanding molecular recognition
between PlGF-1 and Flt-1, highlighting some of
the residues that are critical for receptor recognition.
Mutagenesis analysis, performed on the basis of a structural
model of interaction between PlGF and the minimal
binding domain of Flt-1, has led to the identification
of several PlGF-1 residues involved in Flt-1 recognition.
The two negatively charged residues, Asp-72 and Glu-73,
located in the ?3-?4 loop, are critical for Flt-1 binding.
Other mutations, which bring about a significant decrease
in PlGF binding activity, are Gln-27, located in
the N-terminal ?-helix, and Pro-98 and Tyr-100 on the ?6
strand. The mutation of one of the two glycosylated residues
of PlGF, Asn-84, generates a PlGF variant with
reduced binding activity. This indicates that, unlike in
VEGF, glycosylation plays an important role in Flt-1
binding. The double mutation of residues Asp-72 and
Glu-73 generates a PlGF variant unable to bind and
activate the receptor molecules on the cell surface. This
variant failed to induce in vitro capillary-like tube formation
of primary endothelial cells or neo-angiogenesis
in an in vivo chorioallantoic membrane assay. (literal)
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