The human homologue of the murine Llglh gene (LLGL) maps within the Smith-Magenis syndrome region in 17p11.2

Cytogenet Cell Genet. 1996;72(1):78-82. doi: 10.1159/000134167.

Abstract

We have isolated and characterized the human homologue of the murine Llglh gene, which was originally isolated as a homologue of a Drosophila tumor suppressor gene 1(2)gl (lethal(2) giant larvae). In the mouse, Llglh is thought to play an important role during brain development as a regulatory target of Hoxc8. The human homologue of Llglh (LLGL) encodes a protein consisting of 1,033 amino acids. This gene was mapped by fluorescence in situ hybridization (FISH) to human chromosome 17p11.2, a region that is typically deleted in patients with Smith-Magenis syndrome (SMS). In our FISH analysis of metaphase chromosomes of four SMS patients, a probe representing LLGL failed in each case to hybridize to one of the two chromosome 17 homologues, indicating that this gene may play a role in the pathogenesis of SMS.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Chromosome Mapping
  • Chromosomes, Human, Pair 17*
  • Cytoskeletal Proteins
  • Genes, Tumor Suppressor
  • Humans
  • In Situ Hybridization, Fluorescence
  • Intellectual Disability / genetics
  • Mice
  • Molecular Sequence Data
  • Proteins / genetics*
  • Sequence Alignment
  • Sequence Homology, Nucleic Acid
  • Syndrome

Substances

  • Cytoskeletal Proteins
  • LLGL1 protein, human
  • Proteins

Associated data

  • GENBANK/D50550