Proceedings of the National Academy of Sciences of the United States of America · 2003
Bad-deficient mice develop diffuse large B cell lymphoma.
СтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод пока не подготовлен
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Ranger Ann M, Zha Jiping, Harada Hisashi, Datta Sandeep Robert, Danial Nika N, Gilmore Andrew P, Kutok Jeffery L, Le Beau Michelle M, Greenberg Michael E, Korsmeyer Stanley J
Аннотация
The proapoptotic activity of the "BH3-only" molecule BAD can be differentially regulated by survival factor signaling. Bad-deficient mice lacking both BAD long and BAD short proteins proved viable, and most cell types appeared to develop normally. BAD did not exclusively account for cell death after withdrawal of survival factors, but it was an intermediate for epidermal growth factor- or insulin-like growth factor I-countered apoptosis, consistent with a "sensitizing" BH3-only molecule. Lymphocytes developed normally with no premalignant hyperplasia, but they displayed subtle abnormalities in proliferation and IgG production. Despite the minimal phenotype, Bad-deficient mice progressed, with aging, to diffuse large B cell lymphoma of germinal center origin. Exposure of Bad-null mice to sublethal gamma-irradiation resulted in an increased incidence of pre-T cell and pro-/pre-B cell lymphoblastic leukemia/lymphoma. Thus, proapoptotic BAD suppresses tumorigenesis in the lymphocyte lineage.
Предметные рубрики MeSH
AnimalsApoptosisB-LymphocytesCarrier ProteinsCell DeathCell LineageDNA, ComplementaryExonsGamma RaysImmunoglobulin GKaryotypingLymphoma, B-CellMiceMice, Inbred C57BLMice, KnockoutModels, GeneticNucleic Acid HybridizationPhenotypeProtein BiosynthesisSignal TransductionT-LymphocytesTranscription, Geneticbcl-Associated Death Protein