IndraLab

Statements


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"Reduced BAP1 levels impair DNA repair as well as different forms of cell death and induce metabolic alterations that together favor cancer development and growth."

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"Although this remains to be investigated, these results, suggest that the majority of BAP1 partners regulate SLC7A11 expression and possibility impact ferroptosis.Because ferroptosis and apoptosis are two distinct programs in BAP1-mediated cell death, it will be worth to investigate whether these processes act in concert or independently during cancer development."

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"BAP1 induces cell death via interaction with 14-3-3 in neuroblastoma."

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"- If BAP1 triggers cell death as discussed by the authors , could the authors be selecting for cells with reduced BAP1 knockdown in Fig. S2B ?"

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"Two different strategies were applied to analyze the mechanism of BAP1 inducing cell death in neuroblastoma."

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"Conversely, silencing BAP1 expression reduced the early stage apoptotic cell population to 2.71%, significantly lower than that of the control (5.25%, p < 0.05), suggesting that BAP1 promotes tumor cell death by apoptosis and necrosis."

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"Processes other than apoptosis could be also involved in the cell death mechanism mediated by BaP1 on BAEC and HeLa cell lines [[XREF_BIBR]]."

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"24 For example, BAP1 has been shown to enhance progression through the G1-S checkpoint and subsequently induce cell death by a process with similarities to both apoptosis and necrosis."

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"In contrast, at higher concentrations, BaP1 stains lipid droplets and induces a regulated cell death process mediated by vacuolar membrane permeabilization."

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"For example, BAP1 can enhance progression through the G1-S checkpoint and subsequently induce cell death by a process with similarities to both apoptosis and necrosis [XREF_BIBR]."

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"BAP1 promotes cell death and suppresses cell proliferation in LAC."

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"Under glucose starvation, BAP1 can directly bind to the promoter of ATF3 and CHOP, inhibit its transcription, and thus inhibit the UPR and cell death induced by the ER stress (XREF_FIG p)."

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"Upon culturing fibroblasts for 24 h, we observed that P-I metalloproteinases and LAAO induced approximately 20% and 20-30% cell death respectively."

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"P-I metalloproteinases and LAAO arrested the cells in G0/G1 phase of cell cycle and also led to cytotoxic activity in endothelial cells by inducing necrosis/late apoptotic mode of cell death."

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"P-I metalloproteinases induced cell death of nearly 40% whereas LAAO stimulated 50% cell death after 24 h."

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"Among the most common genetic alterations or deregulated pathways identified in MM, deletions in the cyclin dependent kinase inhibitor 2A (CDKN2A) locus, inactivation of the retinoblastoma (RB) pathway, mutations in the BRCA1 associated protein 1 (BAP1) and neurofibromatosis type 2 (NF2) genes, and aberrant regulation of phosphatidylinositol-4,5- bisphosphate 3-kinase (PI3K)/AKT pathway are all related to MM uncontrolled growth and resistance to treatment induced cell death."

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"More in-depth analysis of BAP1 mediated cell death is warranted in order to determine the specific mechanism of BAP1 mediated growth inhibition."

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"The mechanism that BAP1 induces cell death is mediated via an interaction with 14-3-3 protein."

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"BAP1 promotes cell death in neuroblastoma cells."

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"Processes other than apoptosis could be also involved in the cell death mechanism mediated by BaP1 on BAEC."

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"Our data imply that BAP1 mediated cell death displays properties of both apoptosis and necrosis."

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"We subsequently observed that BAP1 mediated cell death displays features implicating both apoptosis and necrosis."