BH3-only Bcl-2 family member Bim is required for apoptosis of autoreactive thymocytes

By P. Bouillet, J. Purton, D. Godfrey, Li-Chen Zhang, Leigh Coultas, H. Puthalakath, M. Pellegrini, Suzanne Cory, Jerry M. Adams, A. Strasser. Nature, 2002

847 citations recorded by the source corpus.

Subfields: Immunology, Immunology and Allergy, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ae88027d837c518403e4563f7c1a89068b4aae01

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Citations in the corpus

MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “Death receptormediated apoptosis does not appear to play a critical role in thymic central tolerance; however, genetic deletion of members of the BCL-2 family, especially BIM in mice, has shown BIM to be a critical mediator of apoptosis for negative selection in the thymus (Bouillet et al., 2002; St”
Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosome (2002, background): “, deletion of thymocytes with self-reactivity depends on Bi”
Activation‐induced cell death in T cells (2003, background): “A pathway for thymocyte AICD and negative selection has been proposed that does not rely on death receptors at all, but instead it relies on the expression and activation of Bim, a Bcl-2 homology 3-only member of the Bcl-2 family (49).”
Targeted deletion reveals essential and overlapping functions of the miR-17 through 92 family of miRNA clusters. (2008, positive): “Bim belongs to the BH3-only family of proapoptotic genes, and its overexpression leads to apoptosis ( Bouillet et al., 2002; O’Connor et al., 1998).”
Bcl-2-family proteins and the role of mitochondria in apoptosis. (2003, background): “Bim is involved in UV-induced apoptosis, the death of autoreactive thymocytes (negative selection) [41] and in other forms of thymocyte death [42], as well as in the apoptosis of neurons deprived of nerve growth factor (NGF) [43].”
Life in the balance: how BH3-only proteins induce apoptosis. (2005, background): “Bim is crucial not only for eliminating lymphocytes that recognize self-antigens, during the development of both T cells [45] and B cells [46], but also for terminating T cell immune responses [47,48].”
The Bcl-2 apoptotic switch in cancer development and therapy (2007, background): “Bim is also critical for shaping the immune repertoire by eliminating thymocytes that recognize self-antigens (Bouillet et al., 2002) and in terminating T-cell immune responses (Hildeman et al., 2002; Pellegrini et al., 2003).”
ER stress triggers apoptosis by activating BH3-only protein Bim. (2007, background): “, 1999), and is required for deletion of autoreactive T (Bouillet et al., 2002) and B cells (Enders et al.”