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A non-canonical role for BAD and reconciles BAD-mediated tumor growth with favorable outcomes in BAD-high breast cancer patients.
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Targeting BCL-xL improves the efficacy of bromodomain and extra-terminal protein inhibitors in triple-negative breast cancer by eliciting the death of senescent cells.
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High BAD expression is associated with cisplatinresistant oral cancer.
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Bcl-2 agonist of cell death (BAD) has pro-apoptosis and pro-survival functions involved in cancer development [Review].
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The findings suggest that experimental hyperthermia (EH) exposure leads to simultaneous activation of molecular switches of apoptosis (BCL2 and BAD) in cells of the follicular epithelium of the ovaries on days 3 and 4 after EH.
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The positive correlation of Bad expression with nodule size and a relative decrease in the mRNA expression level of Bad in benign thyroid nodules suggest that Bad may be an important regulator of thyroid cell apoptosis.
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Data suggest that ECAD, STAT3, Bak, and Bcl-xL are expressed in affected endometrial tissues of women with endometrioid adenocarcinoma depending on neoplasm staging and cell differentiation. This study was conducted using immunohistochemistry of surgically resected tissues. (ECAD = E-cadherin; STAT3 = signal transducer and activator of transcription 3 protein; Bak = pro-apoptotic protein BAK)
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cyclin D1 was downregulated, whereas Bcell lymphoma 2associated agonist of cell death (BAD) was upregulated following RAC1 knockdown in colon cancer cells.
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we have found that a subgroup of colorectal cancers, defined by having either KRAS or BRAF (KRAS/BRAF) mutations and BCL2L1 (encoding BCL-XL) amplification, can be effectively targeted by simultaneous inhibition of BCL-XL (with ABT-263) and MCL1 (with YM-155).
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BAD phosphorylation is essential in the cytoprotective effect of vasoactive intestinal peptide on cancer stem cells.
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NDRG2 could inhibit Bad degradation by increasing its protein stability in breast cancer cells.
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Taken together, our results provide a structural basis for the binding mechanism between DJ-1 and Bcl-XL, which will contribute to molecular understanding of the role of mitochondrial DJ-1 in Bcl-XL regulation in response to oxidative stress.
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We will then review how the apoptotic and autophagic functions of Bcl-xL are modified by this post-translational modifications, and how this impacts on its oncogenic properties.
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the membrane localization of BCL-xL enforces its control over cell survival and, importantly, limits the pro-apoptotic effects of BH3 mimetics by selectively influencing BCL-xL binding to key pro-apoptotic effectors.
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The long unstructured region of Bcl-xl modulates its structural dynamics.
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Short-term treatment of nascent melanoma tumors with PAK inhibitors that block RhoJ signaling halts the growth of BRAF mutant melanoma tumors in vivo and induces apoptosis in melanoma cells in vitro via a BAD-dependent mechanism. As up to 50% of BRAF mutant human melanomas express high levels of RhoJ, these studies nominate the RhoJ-BAD signaling network as a therapeutic vulnerability for fledgling BRAF mutant human tumor
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Recent studies that combine experiments in yeast and in mammalian cells have shown the unexpected effect of the anti-apoptotic protein Bcl-xL on the priming of Bax. As demonstrated with the BH3-mimetic molecule ABT-737, this property of Bcl-xL, and of Bcl-2, is crucial to elaborate about how apoptosis could be reactivated in tumoral cells.
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the accumulation of reactive oxygen species (ROS) in cells expressing JAK2V617F compromises the NHE-1/Bcl-xL deamidation pathway by repressing NHE-1 upregulation in response to DNA damage. hematopoietic stem cells (HSCs), FOXO3A is largely localized within the nuclei despite the presence of JAK2V617F mutation, suggesting that JAK2-FOXO signaling has a different effect on progenitors compared with stem cells.
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These results identify beta3 integrin signaling via repression of BAD as an important survival pathway used by breast cancer cells to evade chemotherapy induced stress.
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BAD mutation is associated with maturity-onset diabetes of the young.