bcl-2 Homologous Antagonist-Killer Protein
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Subject Areas on Research
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A genome-wide RNAi screen reveals multiple regulators of caspase activation.
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Apoptosis and B cell tolerance.
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Common variants within 6p21.31 locus are associated with chronic lymphocytic leukaemia and, potentially, other non-Hodgkin lymphoma subtypes.
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Deficiency in Bak and Bax perturbs thymic selection and lymphoid homeostasis.
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Dickkopf-1 promotes hematopoietic regeneration via direct and niche-mediated mechanisms.
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ER stress modulates cellular metabolism.
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Epidermal growth factor regulates hematopoietic regeneration after radiation injury.
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Homeostatic control of lymphocyte survival: potential origins and implications.
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Mcl-1 promotes survival of thymocytes by inhibition of Bak in a pathway separate from Bcl-2.
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Mitochondria, cell death, and B cell tolerance.
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Modulation of cytokine-induced cardiac myocyte apoptosis by nitric oxide, Bak, and Bcl-x.
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Persistent fetal ocular vasculature in mice deficient in bax and bak.
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Pro- and antiapoptotic proteins regulate apoptosis but do not protect against cytokine-mediated cytotoxicity in rat islets and beta-cell lines.
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Proapoptotic bcl-2 family members, Bax and Bak, are essential for developmental photoreceptor apoptosis.
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Targeting lysosomal degradation induces p53-dependent cell death and prevents cancer in mouse models of lymphomagenesis.
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The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues.
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Tie2(+) bone marrow endothelial cells regulate hematopoietic stem cell regeneration following radiation injury.
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Tumor cells, but not endothelial cells, mediate eradication of primary sarcomas by stereotactic body radiation therapy.
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p53 controls radiation-induced gastrointestinal syndrome in mice independent of apoptosis.