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Bim/BOD is a group of three splice variants, BimEL, BimL, and BimS, with apparent molecular masses of ~23, 16, and 13 kDa, respectively. Bim is a critical regulator of lymphocyte homeostasis, acts as a barrier against autoimmune disease and is necessary for the apoptotic response to certain stress signals. All isoforms of Bim contain the C-terminal Bcl-2 homology domain known as BH3. Certain apoptotic stimuli release Bim from the complex which allows it to translocate to the mitochondria and bind to Bcl-2 or its homologues, thereby promoting apoptosis.
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Immunohistochemistry analysis of Bim in human skin cancer cells with Bim antibody at 20µg/ml.
Western blot analysis of human K562 cell lysate probed with Bim/BOD, pAb.
Selective impact of 2DG on the BCL-2 protein family. a Abundance of pro-survival and pro-apoptotic proteins of the family, assessed by western blotting, in NALM-6 cells after 6 h of 2DG treatment (1 or 10 mM), showing that only MCL-1 is affected and that mannose (10 mM), but not caspase inhibition (50 μM Q-VD), partially relieves the MCL-1 drop. bMCL-1 mRNA abundance assessed by quantitative RT-PCR in NALM-6 cells treated for 6 h with 2DG (1 or 10 mM) and co-treated as indicated with Q-VD (50 μM) or mannose (10 mM). TRIzol purified mRNA was subjected to random primer RT-PCR, and MCL-1 mRNA level determined by quantitative PCR, normalized by a geometrical mean of four housekeeping mRNAs (GAPDH, TUBβ1, PPIA, and TBP, see Methods). Data are plotted as mean ± SD. Significance was determined by two-way ANOVA: ****P 0.05)
Image collected and cropped by CiteAb under a CC-BY license from the following publication: By reducing global mRNA translation in several ways, 2-deoxyglucose lowers MCL-1 protein and sensitizes hemopoietic tumor cells to BH3 mimetic ABT737. Cell Death Differ (2019)
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RUO – Research Use Only |
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