M Lalande

Summary

Affiliation: University of Connecticut Health Center
Country: USA

Publications

  1. ncbi request reprint Molecular epigenetics of Angelman syndrome
    M Lalande
    Department of Genetics and Developmental Biology, University of Connecticut School of Medicine, Farmington, CT 06030 3301, USA
    Cell Mol Life Sci 64:947-60. 2007
  2. ncbi request reprint The human necdin gene, NDN, is maternally imprinted and located in the Prader-Willi syndrome chromosomal region
    P Jay
    Centre de Recherches de Biochimie Macromoleculaire, CNRS ERS 115, INSERM U 249, Montpellier, France
    Nat Genet 17:357-61. 1997
  3. ncbi request reprint The Angelman syndrome candidate gene, UBE3A/E6-AP, is imprinted in brain
    C Rougeulle
    Nat Genet 17:14-5. 1997
  4. ncbi request reprint UBE3A/E6-AP mutations cause Angelman syndrome
    T Kishino
    Genetics Division, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Genet 15:70-3. 1997
  5. ncbi request reprint FISH ordering of reference markers and of the gene for the alpha 5 subunit of the gamma-aminobutyric acid receptor (GABRA5) within the Angelman and Prader-Willi syndrome chromosomal regions
    J H Knoll
    Genetics Division, Children s Hospital, Boston, MA 02115
    Hum Mol Genet 2:183-9. 1993
  6. pmc High-resolution mapping of the gamma-aminobutyric acid receptor subunit beta 3 and alpha 5 gene cluster on chromosome 15q11-q13, and localization of breakpoints in two Angelman syndrome patients
    D Sinnett
    Genetics Division, Children s Hospital, Boston, MA 02115
    Am J Hum Genet 52:1216-29. 1993
  7. ncbi request reprint Allele specificity of DNA replication timing in the Angelman/Prader-Willi syndrome imprinted chromosomal region
    J H Knoll
    Division of Genetics, Children s Hospital Harvard Medical School, Boston, Massachusetts 02115
    Nat Genet 6:41-6. 1994
  8. ncbi request reprint The syntenic relationship between the critical deletion region for the Prader-Willi/Angelman syndromes and proximal mouse chromosome 7
    J R Chaillet
    Department of Genetics, Harvard Medical School, Boston, Massachusetts
    Genomics 11:773-6. 1991
  9. ncbi request reprint Familial Angelman syndrome caused by imprinted submicroscopic deletion encompassing GABAA receptor beta 3-subunit gene
    S Saitoh
    Lancet 339:366-7. 1992
  10. ncbi request reprint The human MAGEL2 gene and its mouse homologue are paternally expressed and mapped to the Prader-Willi region
    I Boccaccio
    INSERM U491, Faculte de Medecine, 27 Boulevard Jean Moulin, F 13385 Marseille Cedex 5, France
    Hum Mol Genet 8:2497-505. 1999

Collaborators

  • B Horsthemke
  • K Buiting
  • Shinji Saitoh
  • C Rougeulle
  • J Cavaille
  • I Boccaccio
  • N Roeckel
  • F Muscatelli
  • J H Knoll
  • T Kishino
  • P Jay
  • J Wagstaff
  • M Kiefmann
  • A Huttenhofer
  • J Brosius
  • C I Brannan
  • J P Bachellerie
  • D Sinnett
  • F Watrin
  • H Glatt-Deeley
  • H Glatt
  • P Berta
  • A Massacrier
  • A Moncla
  • P Cau
  • P Malzac
  • S Taviaux
  • M G Mattei
  • J L Lefranc
  • K Glatt
  • S D Cheng
  • T Ozcelik
  • J M Sikela
  • E Woolf
  • A S Wilcox
  • E J Kirkness
  • P M Whiting
  • P Wingrove
  • W Robinson
  • J R Chaillet
  • A Schinzel
  • S Leff
  • U Francke
  • T Donlon
  • E Sanjines

Detail Information

Publications12

  1. ncbi request reprint Molecular epigenetics of Angelman syndrome
    M Lalande
    Department of Genetics and Developmental Biology, University of Connecticut School of Medicine, Farmington, CT 06030 3301, USA
    Cell Mol Life Sci 64:947-60. 2007
    ....
  2. ncbi request reprint The human necdin gene, NDN, is maternally imprinted and located in the Prader-Willi syndrome chromosomal region
    P Jay
    Centre de Recherches de Biochimie Macromoleculaire, CNRS ERS 115, INSERM U 249, Montpellier, France
    Nat Genet 17:357-61. 1997
    ..A complete lack of NDN expression in PWS brain and fibroblasts indicates that the gene is expressed exclusively from the paternal allele in these tissues and suggests a possible role of this new gene in PWS...
  3. ncbi request reprint The Angelman syndrome candidate gene, UBE3A/E6-AP, is imprinted in brain
    C Rougeulle
    Nat Genet 17:14-5. 1997
  4. ncbi request reprint UBE3A/E6-AP mutations cause Angelman syndrome
    T Kishino
    Genetics Division, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Genet 15:70-3. 1997
    ..Our results demonstrate that UBE3A mutations are one cause of AS and indicate a possible abnormality in ubiquitin-mediated protein degradation during brain development in this disease...
  5. ncbi request reprint FISH ordering of reference markers and of the gene for the alpha 5 subunit of the gamma-aminobutyric acid receptor (GABRA5) within the Angelman and Prader-Willi syndrome chromosomal regions
    J H Knoll
    Genetics Division, Children s Hospital, Boston, MA 02115
    Hum Mol Genet 2:183-9. 1993
    ..Our results provide a framework map of chromosome 15q11-q13 into which additional markers can be oriented and allow a further differentiation of the critical genetic regions of the two syndromes...
  6. pmc High-resolution mapping of the gamma-aminobutyric acid receptor subunit beta 3 and alpha 5 gene cluster on chromosome 15q11-q13, and localization of breakpoints in two Angelman syndrome patients
    D Sinnett
    Genetics Division, Children s Hospital, Boston, MA 02115
    Am J Hum Genet 52:1216-29. 1993
    ..These findings will facilitate chromosomal walking strategies for cloning the regions disrupted by the DNA rearrangements in these AS patients and will be valuable for mapping new genes to the AS chromosomal region...
  7. ncbi request reprint Allele specificity of DNA replication timing in the Angelman/Prader-Willi syndrome imprinted chromosomal region
    J H Knoll
    Division of Genetics, Children s Hospital Harvard Medical School, Boston, Massachusetts 02115
    Nat Genet 6:41-6. 1994
    ..At the most distal locus examined, D15S12, both patterns of allele-specific replication timing were detected...
  8. ncbi request reprint The syntenic relationship between the critical deletion region for the Prader-Willi/Angelman syndromes and proximal mouse chromosome 7
    J R Chaillet
    Department of Genetics, Harvard Medical School, Boston, Massachusetts
    Genomics 11:773-6. 1991
    ..Because the Prader-Willi and Angelman syndromes are postulated to result from genomic imprinting within the common deletion, these probes may define a genomically imprinted region on mouse chromosome 7...
  9. ncbi request reprint Familial Angelman syndrome caused by imprinted submicroscopic deletion encompassing GABAA receptor beta 3-subunit gene
    S Saitoh
    Lancet 339:366-7. 1992
  10. ncbi request reprint The human MAGEL2 gene and its mouse homologue are paternally expressed and mapped to the Prader-Willi region
    I Boccaccio
    INSERM U491, Faculte de Medecine, 27 Boulevard Jean Moulin, F 13385 Marseille Cedex 5, France
    Hum Mol Genet 8:2497-505. 1999
    ..Moreover, MAGEL2 / Magel2 are expressed only from the paternal allele in brain, suggesting a potential role in the aetiology of PWS and its mouse model, respectively...
  11. pmc Identification of brain-specific and imprinted small nucleolar RNA genes exhibiting an unusual genomic organization
    J Cavaille
    Laboratoire de Biologie Mol├ęculaire Eukaryote du Centre National de la Recherche Scientifique, Universite Paul Sabatier, Toulouse, 31062 France
    Proc Natl Acad Sci U S A 97:14311-6. 2000
    ..Instead, brain-specific C/D box snoRNA HBII-52 has an 18-nt phylogenetically conserved complementarity to a critical segment of serotonin 2C receptor mRNA, pointing to a potential role in the processing of this mRNA...
  12. ncbi request reprint Small nuclear ribonucleoprotein polypeptide N (SNRPN), an expressed gene in the Prader-Willi syndrome critical region
    T Ozcelik
    Howard Hughes Medical Institute, Stanford University School of Medicine, California 94305
    Nat Genet 2:265-9. 1992
    ..The fact that the mouse Snrpn gene is maternally imprinted in brain suggests that loss of the paternally derived SNRPN allele may be involved in the PWS phenotype...