IndraLab

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"Liu et al. reported that USP29 expression was elevated upon oxidative stress and then promoted cell apoptosis via directly deubiquitinating p53 [25]."
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"Recently , a study reported that USP29 depletion decreased apoptosis by regulating the Snail protein [ 13 ] ."
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"We also demonstrated that USP29 depletion hampers the colony formation and increases apoptosis of HCT116 cells."
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"Collectively, these findings imply that USP29 potentiates I/R-induced oxidative damage and neuronal apoptosis in vitro."
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"Neuron-specific USP29 knockout significantly diminishes, whereas USP29 overexpression aggravates cerebral I/R-induced oxidative stress, apoptosis, and neurological dysfunction in vivo and in vitro."
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"Based on the above results, we conclude that USP29 upregulation during cerebral I/R injury potentiates oxidative stress, apoptosis, and neurological dysfunction in mice."
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"Generally, our findings for the first time identify that USP29 upregulation during cerebral I/R may contribute to oxidative stress, neuronal apoptosis, and the progression of cerebral I/R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I/R injury.Multiple mechanisms are implicated in the pathogenesis of cerebral I/R injury, including oxidative stress and apoptosis."
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"Neuron-specific USP29 knockout significantly diminished, whereas USP29 overexpression aggravated cerebral I/R-induced oxidative stress, apoptosis, and neurological dysfunction in mice."
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"In addition, OGD/R-induced oxidative stress and neuronal apoptosis were also attenuated by USP29 silence but exacerbated by USP29 overexpression in vitro."
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"Our findings for the first time identify that USP29 upregulation during cerebral I/R may contribute to oxidative stress, neuronal apoptosis, and the progression of cerebral I/R injury and that inhibition of USP29 may help to develop novel therapeutic strategies to treat cerebral I/R injury."
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"During stress, USP29 removes the polyubiquitin chain from p53 thus stabilizing it and induces p53 dependent apoptosis."
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