2004
Hypermutability in a Drosophila model for multiple endocrine neoplasia type 1
Busygina V, Suphapeetiporn K, Marek LR, Stowers RS, Xu T, Bale AE. Hypermutability in a Drosophila model for multiple endocrine neoplasia type 1. Human Molecular Genetics 2004, 13: 2399-2408. PMID: 15333582, DOI: 10.1093/hmg/ddh271.Peer-Reviewed Original ResearchConceptsDNA cross-linking agentsNucleotide excision repairDNA damage-induced mutationsTumor suppressor geneDamage-induced mutationsDrosophila homologGenomic integrityHuman meninMutant fliesBiochemical functionsTranscriptional modulationNuclear proteinsDrosophila modelProtein 50Novel memberExcision repairNull allelesMolecular mechanismsCancer genesHistone deacetylaseSuppressor geneHomozygous inactivationMnn1Normal fliesGenes
2002
MEN1 tumor‐suppressor protein localizes to telomeres during meiosis
Suphapeetiporn K, Greally JM, Walpita D, Ashley T, Bale AE. MEN1 tumor‐suppressor protein localizes to telomeres during meiosis. Genes Chromosomes And Cancer 2002, 35: 81-85. PMID: 12203793, DOI: 10.1002/gcc.10113.Peer-Reviewed Original ResearchConceptsSomatic cellsTelomerase activityAbsence of meninTumor suppressor gene MEN1Normal cell physiologyTelomeric protein TRF2Normal telomerase activityTumor suppressor proteinRole of meninMeiotic telomeresTelomere functionProtein TRF2Meiotic cellsTranscriptional activationNuclear proteinsCell physiologyFunctional motifsDifferent proteinsTumor suppressorTelomeresMeninElevated telomerase activityDifferent tissuesJunDCancer predisposition syndrome