IndraLab

Statements



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"Our study revealed that Jab1 depletion contributes to increased UV and IR and cisplatin sensitivity by increasing DNA damage and suppressing DNA repair, which in turn, contributes to an increase in cisplatin-, IR-, and UV induced apoptosis."

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"Consistent with impaired HR function in Jab1 knockdown cells, we also found that Jab1 +/- MEFs, compared with wild-type MEFs, significantly increased cell death in response to death stimuli UV IR and gamma-IR (XREF_FIG)."

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"The current finding that Jab1 positively regulates Rad51 and contributes to the response of NPC cells to cisplatin, IR and UV suggests that assessing the Jab1 level in patients may help predict response to cisplatin and radiation treatments, allowing the design of individualized treatment strategies for patients with NPC."

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"By contrast, exogenous Jab1 expression enhanced the resistance of NPC cells to cisplatin, IR and UV Moreover, we provide a mechanism by which Jab1 positively regulated Rad51 through p53 dependent pathway, and increased ectopic expression of Rad51 conferred cellular resistance to cisplatin, IR and UV in Jab1 deficient cells."

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"By contrast, exogenous Jab1 expression enhanced the resistance of NPC cells to cisplatin, IR and UV radiation."

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"In comparison, the levels of expression of Ku70, known to be an important protein in the NHEJ DNA-repair pathway, and of phospho-Chk2, a key molecule in the transduction of DNA damage signaling induced by DSBs [XREF_BIBR, XREF_BIBR], were increased after IR exposure regardless of whether the cells were treated with Jab1 and CSN5 or control siRNA."

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"These observations suggested that Jab1 and CSN5 is a major contributor to the resistance of NPC to UV radiation, IR, and cisplatin."

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"On the basis of our previous findings, we hypothesized that Jab1 contributes to cisplatin, IR and UV resistance."