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Characterization of a Novel ARID Family Member, ARID3C (Brightlike)
Author(s) -
Curcio Josephine Antonette,
Probst Loren,
Tucker Philip
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.408
Subject(s) - biology , sumo protein , gene , chromatin , rna splicing , locus (genetics) , genetics , microbiology and biotechnology , alternative splicing , subfamily , genome , messenger rna , rna , ubiquitin
ARID proteins are highly conserved among eukaryotes and are involved in chromatin remodeling, differentiation and development. The founding member of the ARID3 subfamily, Bright/ARID3A, is an activator of the immunoglobulin heavy chain locus. Bright interacts with sumoylation E2 (UBC9) and E3 (PIAS1) components and undergoes modification by SUMO‐1. Bright has been shown to immortalize mouse embryonic fibroblasts and induce malignant transformation when co‐expressed with oncogenic Ras. A genomic locus that encodes a gene paralogous to Bright has been identified as Brightlike/ARID3C. In addition to the highly conserved ARID and REKLES domains, Brightlike contains a conserved sumoylation motif. Brightlike orthologous genes have been identified in all vertebrate genomes examined. Its absence from EST databases suggested that it is a rare transcript, and accordingly, its expression in adult mice appears to be restricted to spleen, testes and thymus. Brightlike is also regulated by alternative pre‐mRNA splicing and differential subcellular distribution. Brightlike and Bright bind to the same DNA motif. Unexpectedly, Bright and Brightlike do not form heterocomplexes on DNA nor compete for binding, suggesting they have independent functions in vivo. Current goals address this issue, whether over‐expression of Brightlike leads to malignant transformation, and the functional consequences of sumoylation.