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OTUD7B inhibits apoptotic process. 14 / 14
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"We found that Cezanne overexpression in NRCMs activated AKT/mTOR to reduce apoptosis, autophagy and oxidative stress; this mechanism of Cezanne was also verified in animal experiments."
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"OTUD7B (Cezanne) prevents tumor necrosis factor (TNF)-induced apoptosis of dendric cells in infection (Harit et al. 2023) and facilitates T cell activation and inflammatory responses by regulating Zap70 ubiquitination (Hu et al. 2016)."
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"Western blot indicated that AAV9-Cezanne decreased the ratio of Bax to Bcl-2 and further confirmed that Cezanne could inhibit cardiomyocyte apoptosis ( Fig. 6 D)."
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"These results indicated that OTUD7B knockdown promoted apoptosis in PC3 cells."
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"OTUD7B knockdown effectively induced apoptosis and inhibited the proliferation in PC3 cells."
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"Our animal experiments revealed that Cezanne overexpression in mice reversed DOX-induced cardiomyocyte apoptosis, autophagy, oxidative stress and hypertrophy."
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"Taken together, OTUD7B promotes the proliferation, and autophagy, and inhibits apoptosis of prostate cancer cells via the AKT/mTOR signaling pathway."
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"OTUD7b stabilizes TRAF2 by cleaving K48-linked polyubiquitin chains and prevents DC apoptosis."
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"16 , 17 Molecularly, OTUD7B inhibits LCL161 inhibitor of apoptosis protein antagonist‐induced invasion and migration by binding to and deubiquitinating TRAF3 (tumor necrosis factor receptor‐associated factor 3), thereby inhibiting NIK (NF‐κB‐inducing kinase) and preventing noncanonical NF‐κB activation in lung cancer."
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"Therefore, we transfected Ad-shCezanne to knock down Cezanne levels and found that Cezanne knockdown significantly promoted DOX-induced apoptosis in NRCMs via Western blot ( Fig. 3 A)."
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"Subsequent functional experiments found that Cezanne knockdown in NRCMs promoted DOX-induced apoptosis, autophagy and oxidative stress, while Cezanne overexpression protected NRCMs from these damages [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Additionally, OTUD7B knockdown was found to induce apoptosis in PC3 cells."
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"OTUD7B knockdown increased the apoptosis rate, as shown by annexin V/PI staining and the expression of cleaved-caspase 9, cleaved-caspase 3, and PARP-1 (Fig. 2D and E)."
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"However, combined pharmacological inhibition of RIPK1 activity (Nec1s) and apoptosis (zVAD-FMK) completely rescued survival of OTUD7b-deficient BMDC in vitro and in vivo indicating that OTUD7b inhibits RIPK1-independent and to a lesser extent RIPK1-dependent DC apoptosis [43]."
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