IndraLab

Statements

KCNK2 inhibits apoptotic process. 9 / 9
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"The over-expression of TREK1 could decrease apoptosis and NADH in neurons."
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"However, blockade of TREK1 channels raised the number of hypoxia induced neuronal apoptosis in a neuron-astrocyte co-culture indicating a neuroprotective role of TREK1 channels after hypoxia [XREF_BIBR]."
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"Kcnk2 overexpression enhanced the viability and inhibited the apoptosis of the H/R-treated PC12 cells."
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"Taken together, this result indicated that the over-expression of TREK1 might reduce the apoptosis of neurons to play a role of neuroprotection."
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"Foxd3 upregulated miR-214 which can inhibit the expression of Kcnk2, thus resulting in reduced viability and increased apoptosis of PC12 cells under hypoxia/reoxygenation conditions."
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"The evaluation of cell viability (Fig. 1d), apoptosis (Fig. 1e) and the expression of Kcnk2, Bax and Ki67 (Fig. 1f) revealed that the H/R treatment significantly reduced the cell viability and Kcnk2 and Ki67 protein expression, while promoting apoptosis and the expression of Bax in PC12 cells compared to control cells (p < 0.05)."
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"For instance, some KCNK2 modulators inhibit apoptosis and promote proliferation in ovarian cancer [14]."
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"In addition, upregulation of Kcnk2 or knockdown of Foxd3 promoted the cell viability and reduced the apoptosis of the H/R treated PC12 cells."
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"The results indicated that TREK1 could decrease neurons apoptosis caused by hypoxia or ischemia."
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