Cell · 1999
Bcl10 is involved in t(1;14)(p22;q32) of MALT B cell lymphoma and mutated in multiple tumor types.
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Willis T G, Jadayel D M, Du M Q, Peng H, Perry A R, Abdul-Rauf M, Price H, Karran L, Majekodunmi O, Wlodarska I, Pan L, Crook T, Hamoudi R, Isaacson P G, Dyer M J
Аннотация
MALT B cell lymphomas with t(1;14)(p22;q32) showed a recurrent breakpoint upstream of the promoter of a novel gene, Bcl10. Bcl10 is a cellular homolog of the equine herpesvirus-2 E10 gene: both contain an amino-terminal caspase recruitment domain (CARD) homologous to that found in several apoptotic molecules. Bcl10 and E10 activated NF-kappaB but caused apoptosis of 293 cells. Bcl10 expressed in a MALT lymphoma exhibited a frameshift mutation resulting in truncation distal to the CARD. Truncated Bcl10 activated NF-kappaB but did not induce apoptosis. Wild-type Bcl10 suppressed transformation, whereas mutant forms had lost this activity and displayed gain-of-function transforming activity. Similar mutations were detected in other tumor types, indicating that Bcl10 may be commonly involved in the pathogenesis of human malignancy.
Предметные рубрики MeSH
Adaptor Proteins, Signal TransducingAmino Acid SequenceAnimalsApoptosisB-Cell CLL-Lymphoma 10 ProteinBase SequenceCOS CellsCell Line, TransformedCell Transformation, NeoplasticChromosomes, Human, Pair 1Chromosomes, Human, Pair 14Cloning, MolecularGene ExpressionHeLa CellsHumansLymphoma, B-Cell, Marginal ZoneMiceMolecular Sequence DataMutationNF-kappa BNeoplasm ProteinsNeoplasmsSequence Homology, Amino AcidTranslocation, Genetic