A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Interspliced transcription chimeras: Neglected pathological mechanism infiltrating gene accession queries?
Tekijät: Tolvanen Martti; Ojala Pauli J.; Törönen Petri; Anderson Heidi; Partanen Jukka; Turpeinen Hannu
Kustantaja: Elsevier BV
Julkaisuvuosi: 2009
Journal: Journal of Biomedical Informatics
Tietokannassa oleva lehden nimi: Journal of Biomedical Informatics
Lehden akronyymi: J Biomed Inform
Vuosikerta: 42
Numero: 2
Aloitussivu: 382
Lopetussivu: 389
ISSN: 1532-0464
eISSN: 1532-0480
DOI: https://doi.org/10.1016/j.jbi.2008.11.002
Verkko-osoite: https://doi.org/10.1016/j.jbi.2008.11.002
Tiivistelmä
Over half of the DNA of mammalian genomes is transcribed, and one of the emerging enigmas in the field of RNA research is intergenic splicing or transcription induced chimerism. We argue that fused low-copy-number transcripts constitute neglected pathological mechanism akin to copy number variation, due to loss of stoichiometric subunit ratios in protein complexes. An obstacle for transcriptomics meta-analysis of published microarrays is the traditional nomenclature of merged transcript neighbors under same accession codes. Tandem transcripts cover 4-20% of genomes but are only loosely overlapping in population. They were most enriched in systems medicine annotations concerning neurology, thalassemia and genital disorders in the GeneGo Inc. MetaCore-MetaDrug(TM) knowledgebase, evaluated with external randomizations here. Clinical transcriptomics is good news since new disease etiologies offer new remedies. We identified homeotic HOX-transfactors centered around BMI-1, the Grb2 adaptor network, the kallikrein system, and thalassemia RNA surveillance as vulnerable hotspot chimeras. As a cure, RNA interference would require verification of chimerism from symptomatic tissue contra healthy control tissue from the same patient.
Over half of the DNA of mammalian genomes is transcribed, and one of the emerging enigmas in the field of RNA research is intergenic splicing or transcription induced chimerism. We argue that fused low-copy-number transcripts constitute neglected pathological mechanism akin to copy number variation, due to loss of stoichiometric subunit ratios in protein complexes. An obstacle for transcriptomics meta-analysis of published microarrays is the traditional nomenclature of merged transcript neighbors under same accession codes. Tandem transcripts cover 4-20% of genomes but are only loosely overlapping in population. They were most enriched in systems medicine annotations concerning neurology, thalassemia and genital disorders in the GeneGo Inc. MetaCore-MetaDrug(TM) knowledgebase, evaluated with external randomizations here. Clinical transcriptomics is good news since new disease etiologies offer new remedies. We identified homeotic HOX-transfactors centered around BMI-1, the Grb2 adaptor network, the kallikrein system, and thalassemia RNA surveillance as vulnerable hotspot chimeras. As a cure, RNA interference would require verification of chimerism from symptomatic tissue contra healthy control tissue from the same patient.
Turun yliopiston Tutkimustietojärjestelmän portaali