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