Umberto Galderisi

Professor of Molecular Biology

Name Umberto
Surname Galderisi
Institution Università degli Studi della Campania Luigi Vanvitelli
Telephone +39 081 566 75 85
E-Mail umberto.galderisi@unicampania.it
Address Dept. of Experimental Medicine, Via Luigi De Crecchio 7 – 80138 Napoli, Italy
Umberto Galderisi

PersonalLinks

Member PUBLICATIONS

  • CTG repeat number in the nonaffected allele of myotonic dystrophy patients is not critical for disease expression.

    Publication Date: 01/12/1997 on Human biology
    by Cipollaro M, Galderisi U, Iacomino G, Galano G, Di Bernardo G, Lus G, Cotrufo R, Orsini A, Santoro L, Pastore L, Sarrantonio C, Salvatore F, Cascino A

    To investigate whether unusual allele segregation might explain the dominant negative effect of the expanded allele for myotonic dystrophy on myotonin protein kinase mRNA metabolism, which is suggested to cause the disease, we determined the number of CTG repeats at the DM locus in the nonaffected alleles of 64 DM (dystrophia myotonia) patients. The relative distribution was then compared with the distributions obtained from alleles of the normal parents and normal siblings of DM patients. Comparison was also made with the allele distribution of normal subjects from the same geographic area. It appears that the CTG repeat number of the nonaffected allele in DM patients is not critical for the expression of the disease.

  • Myotonic dystrophy: antisense oligonucleotide inhibition of DMPK gene expression in vitro.

    Publication Date: 25/04/1996 on Biochemical and biophysical research communications
    by Galderisi U, Cipollaro M, Melone MA, Iacomino G, Di Bernardo G, Galano G, Contrufo R, Zappia V, Cascino A
    DOI: 10.1006/bbrc.1996.0668

    Antisense phosphorothioate oligonucleotides, targeted against the first codon starting region of DMPK mRNA, were successfully used in K562 and HepG2 cells to decrease DMPK expression. The most effective antisense oligo, MIO1, when added to K562 cells, shows a 75% reduction of the DMPK gene expression 6 hours after addition. The same molecule, when encapsulated in liposomes, delays myotonin mRNA decrease at 24 hours after cell treatment. This considerable success with such inhibition in vitro could be utilised to generate a cell model to study myotonic dystrophy (DM) chemio-physiological alterations.

  • Gross reversal of brain parieto-occipital asymmetry in a case of DSM IV simple schizophrenia.

    Publication Date: 01/02/1995 on Schizophrenia research
    by Maj M, Galderisi S, Conforti R, Colucci D'Amato A