IndraLab

Statements


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"Thus, in our next experiments we determined whether loss of Jab1 promotes apoptosis of NPC cells in response to DNA damage."

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"These results suggest that Jab1 depletion spontaneously induces DNA damage and increases the anti-proliferative and anti-migratory effects of DNA damaging agents.In colorectal cancer cell lines, Jab1 silencing decreased p38 and AKT phosphorylation [25]."

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"Loss of Jab1 sensitized cells to gamma radiation induced apoptosis and increased spontaneous DNA damage and homologous recombination defects."

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"Jab1 knockdown produced anti-proliferative and anti-migratory effects in BTC cells by increasing DNA damage, stabilizing PTEN, and leading to G1 cell cycle arrest."

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"Inhibition of CSN5 induced significant DNA damage through inhibition of DNA repair genes in PC cells (Figs."

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"Inhibition of CSN5 in PC cells can induce DNA damage marker activation, including phosphorylation of ATM and H2A.X (Fig. 3D) and DNA repair gene RAD51 reduction (Fig. 3E)."

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"Consistent with other studies, we demonstrated that CSN5 inhibition induced significant DNA damage by inhibition of multiple DNA repair genes (eg, RAD51, ZWINT, BRCA1, and BRCA2)."

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"These results indicate that Jab1/CSN5 deficiency enhances DNA damage and decreases DNA repair after exposure to DNA damage stimuli.An interesting connection between Jab1/CSN5 and the hypoxia-inducible[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"