Development and maintenance of B and T lymphocytes requires antiapoptotic MCL-1
By J. Opferman, A. Letai, C. Beard, M. Sorcinelli, C. Ong, S. Korsmeyer. Nature, 2003
855 citations recorded by the source corpus.
Subfields: Ecology, Nature and Landscape Conservation, Plant Science
View Paper: https://www.semanticscholar.org/paper/b5fcda6fd9a47d7ef14b8e3e8c80c00fde1b990a
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Citations in the corpus
- The Bcl-2 apoptotic switch in cancer development and therapy (2007, background): “…for the survival and implantation of the zygote (Rinkenberger et al., 2000), and its conditional elimination has revealed critical roles in B and T lymphopoiesis and early hematopoiesis (Opferman et al., 2003, 2005), as well as in mature neutrophils but not macrophages (Dzhagalov et al., 2006).”
- Control of mitochondrial apoptosis by the Bcl-2 family (2009, background): “In fact, there are data that support the role of Puma, p53 and heat as activators of Bax and Bak (Chipuk et al., 2004; Kim et al., 2006; Pagliari et al., 2005), and possibly others remain undiscovered.”
- Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins. (2005, background): “Similarly, the marked degeneration of lymphoid cells with mcl-1 conditionally deleted (Opferman et al. 2003) would be attributable to the minimal levels of Bcl-xL found at particular stages of B- and T-cell development (Marsden and Strasser 2003), and the decimation of myeloid progenitor and stem ce”
- Glycogen synthase kinase-3 regulates mitochondrial outer membrane permeabilization and apoptosis by destabilization of MCL-1. (2006, background): “Induction of mcl-1 mRNA by growth factors has been shown to be transient upon growth factor stimulation (Opferman et al., 2003).”
- mir-29 regulates Mcl-1 protein expression and apoptosis (2007, background): “For example, conditional deletion of Mcl-1 results in bone marrow failure due to inappropriate apoptosis of precursor cells (Opferman et al., 2003), whereas transgenic mice with constitutive Mcl-1 expression develop hematologic malignancies (Zhou et al.”
- Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members. (2006, background): “Consistent with our binding chart, we have shown that MCL-1 preferentially binds BIM but not BAD, governing murine lymphocyte dependence on MCL-1 for survival (Opferman et al., 2003).”
- Deubiquitinase USP9X stabilizes MCL1 and promotes tumour cell survival (2010, methodology): “The association of USP9X mRNA expression with prognostic outcome was tested in two different ways: by treating the expression value (1) as a continuous variable, or (2) as a categorical variable.”