Erika Nieddu

Summary

Affiliation: University of Genoa
Country: Italy

Publications

  1. ncbi request reprint Sequence specific peptidomimetic molecules inhibitors of a protein-protein interaction at the helix 1 level of c-Myc
    Erika Nieddu
    Department of Pharmaceutical Sciences, University of Genoa, Viale Benedetto XV, Genoa 16132, Italy
    FASEB J 19:632-4. 2005
  2. ncbi request reprint Interfering with protein-protein contact: molecular interaction maps and peptide modulators
    Erika Nieddu
    Department of Pharmaceutical Sciences, University of Genoa, 16132 Genoa, Italy
    Curr Top Med Chem 7:21-32. 2007
  3. doi request reprint The search for a common structural moiety among selected pharmacological correctors of the mutant CFTR chloride channel
    Erika Nieddu
    Department of Pharmacy, University of Genova, Viale Benedetto XV, 3 16132 Genova, Italy
    Future Med Chem 6:1857-68. 2014
  4. ncbi request reprint 2-(dialkylamino)-4H-1-benzopyran-4-one derivatives modify chloride conductance in CFTR expressing cells
    Mauro Mazzei
    Dipartimento di Scienze Farmaceutiche, Viale Benedetto XV, 3 16132 Genoa, Italy
    Farmaco 58:961-70. 2003
  5. ncbi request reprint F508del-CFTR rescue: a matter of cell stress response
    Erika Nieddu
    Pharmacy Department, University of Genoa, Viale Benedetto XV 3, Genoa, Italy
    Curr Pharm Des 19:3476-96. 2013
  6. doi request reprint Asymmetric 4-aryl-1,4-dihydropyridines potentiate mutant cystic fibrosis transmembrane conductance regulator (CFTR)
    Michele Giampieri
    Department of Pharmacy, University of Genova, Viale Benedetto XV, 3, 16132 Genova, Italy
    ChemMedChem 7:1799-807. 2012
  7. ncbi request reprint Activity of Mannich bases of 7-hydroxycoumarin against Flaviviridae
    Mauro Mazzei
    Department of Pharmaceutical Sciences, Viale Benedetto XV, 3, 16132 Genova, Italy
    Bioorg Med Chem 16:2591-605. 2008
  8. ncbi request reprint Antihypertensive 1,4-dihydropyridines as correctors of the cystic fibrosis transmembrane conductance regulator channel gating defect caused by cystic fibrosis mutations
    Nicoletta Pedemonte
    Laboratorio di Genetica Molecolare, Istituto Giannina Gaslini, L go Gerolamo Gaslini, 5, 16147 Genova, Italy
    Mol Pharmacol 68:1736-46. 2005

Detail Information

Publications8

  1. ncbi request reprint Sequence specific peptidomimetic molecules inhibitors of a protein-protein interaction at the helix 1 level of c-Myc
    Erika Nieddu
    Department of Pharmaceutical Sciences, University of Genoa, Viale Benedetto XV, Genoa 16132, Italy
    FASEB J 19:632-4. 2005
    ..RI-Int-H1-S6A,F8A-loop-H2 was less active rather than more active in respect to RI-Int-VV-H1-S6A,F8A, apparently because it has a clear bent to form a beta-sheet (CD and NMR data)...
  2. ncbi request reprint Interfering with protein-protein contact: molecular interaction maps and peptide modulators
    Erika Nieddu
    Department of Pharmaceutical Sciences, University of Genoa, 16132 Genoa, Italy
    Curr Top Med Chem 7:21-32. 2007
    ..Therefore, peptides mimicking the interacting zone can be considered as potential leads in the rational design of effective molecules. Here different examples of peptides as protein-protein interaction inhibitors are reported...
  3. doi request reprint The search for a common structural moiety among selected pharmacological correctors of the mutant CFTR chloride channel
    Erika Nieddu
    Department of Pharmacy, University of Genova, Viale Benedetto XV, 3 16132 Genova, Italy
    Future Med Chem 6:1857-68. 2014
    ..The F508del mutation impairs the trafficking of CFTR from endoplasmic reticulum to plasma membrane and is responsible of a severe form of cystic fibrosis. Trafficking can be improved by small organic molecules called 'correctors'...
  4. ncbi request reprint 2-(dialkylamino)-4H-1-benzopyran-4-one derivatives modify chloride conductance in CFTR expressing cells
    Mauro Mazzei
    Dipartimento di Scienze Farmaceutiche, Viale Benedetto XV, 3 16132 Genoa, Italy
    Farmaco 58:961-70. 2003
    ..Among the tested compounds the dinitrile derivatives 8 and 9 are endowed with an activity comparable to the reference compound apigenin...
  5. ncbi request reprint F508del-CFTR rescue: a matter of cell stress response
    Erika Nieddu
    Pharmacy Department, University of Genoa, Viale Benedetto XV 3, Genoa, Italy
    Curr Pharm Des 19:3476-96. 2013
    ..The identification of a common mechanism of action for different types of correctors could drive the discovery of new active molecules in CF, overcoming methods clinically inapplicable, such as the low temperature...
  6. doi request reprint Asymmetric 4-aryl-1,4-dihydropyridines potentiate mutant cystic fibrosis transmembrane conductance regulator (CFTR)
    Michele Giampieri
    Department of Pharmacy, University of Genova, Viale Benedetto XV, 3, 16132 Genova, Italy
    ChemMedChem 7:1799-807. 2012
    ..It is probable that the degree of DHP asymmetry considered in our analysis is still insufficient with respect to that allowed in a putative DHP binding site in CFTR, so that the site could equally accommodate both enantiomers...
  7. ncbi request reprint Activity of Mannich bases of 7-hydroxycoumarin against Flaviviridae
    Mauro Mazzei
    Department of Pharmaceutical Sciences, Viale Benedetto XV, 3, 16132 Genova, Italy
    Bioorg Med Chem 16:2591-605. 2008
    ..The good correlation between calculated molecular modeling IC(50) and experimental EC(50) indicates that DNA polymerase is potentially involved in the inhibition of surrogate HCV viruses...
  8. ncbi request reprint Antihypertensive 1,4-dihydropyridines as correctors of the cystic fibrosis transmembrane conductance regulator channel gating defect caused by cystic fibrosis mutations
    Nicoletta Pedemonte
    Laboratorio di Genetica Molecolare, Istituto Giannina Gaslini, L go Gerolamo Gaslini, 5, 16147 Genova, Italy
    Mol Pharmacol 68:1736-46. 2005
    ..DHP activity was confirmed in airway epithelial cells from patients with CF. DHPs may represent a novel class of therapeutic agents able to correct the defect caused by a set of CF mutations...