IndraLab

Statements


COPS5 activates RAD51. 10 / 10
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"Jab1 positively regulates Rad51 through p53 pathway."

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"In this study, we used three NPC cell lines (CNE1, CNE2, and HONE1) to investigate the hypothesis that Jab1 positively regulates the DNA repair protein Rad51 and, in turn, cellular response to treatment with DNA damaging agents such as cisplatin, ionizing radiation (IR) and ultraviolet (UV)."

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"Furthermore, Jab1 positively regulates Rad51 in NPC, explaining why Jab1 depletion sensitizes NPC cells to cisplatin, IR and UV."

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"Liu et al 's study 29 showed that Jab1 contributes to chemoresistance in breast cancer by regulating Rad51, and patients with Jab1 overexpression exhibited a poor prognosis."

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"Transient knockdown of JAB1 by siRNA decreased Rad51 promoter activity in U2OS (p53 WT) cells but not in Saos-2 (p53-null) cells (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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"Recently, we found that Jab1 and Csn5 positively regulates the DNA repair gene Rad51 and contributes to radiation resistance in NPC; Therefore, we hypothesized that Jab1 and Csn5 participates in the process of recurrence after radical radiotherapy in NPC patients."

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"Thus, we hypothesized that Jab1 depletion may impair Rad51 activity, which in turn increases chemosensitivity and chemotherapy-induced apoptosis."

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"Recently, we found that the aberrant activation of Jab1 overexpression is correlated with a lower survival rate in NPC patients 14 and that Jab1 positively regulates the DNA repair gene Rad51 and contributes to NPC cells ' response to radiotherapy and cisplatin 15."

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"Further, Jab1 positively regulates Rad51 in breast cancer, which explains why Jab1 depletion sensitizes breast cancer cells to adriamycin and cisplatin."