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USP11 is involved in chromatin condensation, genomic stability, and cell survival. Together, these observations indicate that USP11 is a chromatin modifier critically involved in DNA damage response and the maintenance of genomic stability.
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USP11 depletion suppresses cell proliferation and wound healing in lung epithelial cells, and these effects are reversed by E2F1 and PEG10 overexpression.
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A crystal structure of a USP11-peptide complex revealed a previously unknown binding site in USP11's noncatalytic ubiquitin-like region.
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modulating USP11 expression altered the stability of TGFb receptor type II (TGFBR2) and TGFb downstream signaling in human breast cancer cells. Together, these data suggest that deubiquitination of TGFBR2 by USP11 effectively spares TGFBR2 from proteasomal degradation to promote EMT and metastasis
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Studied ubiquitin specific peptidase 11 (USP11) expression in hepatocellular carcinoma in clinical samples, in vivo and in vitro; found USP11 upregulated HCC cell invasion, migration ability and results suggest USP11 promotes HCC tumor invasion through inducing angiogenesis.
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Study results revealed that USP11 promoted epithelialtomesenchymal transition in ovarian cancer by deubiquitinating Snail, and USP11 may be a novel therapeutic target for ovarian cancer treatment.
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FASN-induced S6 kinase facilitates USP11-eIF4B complex formation for sustained oncogenic translation in diffuse large B-cell lymphoma.
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These findings reveal an important mechanism by which p21 can be stabilized by direct deubiquitylation, and they pinpoint a crucial role of the USP11-p21 axis in regulating cell-cycle progression and DNA damage responses.
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show that USP11 is associated with the mitotic spindle, does not regulate SAC inactivation, but controls ubiquitination of RAE1 at the mitotic spindle, hereby functionally modulating its interaction with Nuclear Mitotic Apparatus protein (NuMA)
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High USP11 expression is associated with cancer.
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USP11 may contribute to the pathogenesis of pulmonary fibrosis by stabilization of TbetaRII and promotion of TGFbeta-1 signaling.
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We demonstrated that, while depletion of XIAP attenuates cell transformation, elevated USP11 significantly promotes the tumor colony formation through stabilization of XIAP.
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These findings elucidate deeply and extensively the mechanism of RNF8/RNF168 and USP11 to maintain the proper status of ubiquitylation gammaH2AX to repair double strand breaks.
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novel insight into cross-talk between ubiquitin and SUMO and uncover USP11 and RNF4 as a balanced SUMO-targeted ubiquitin ligase/protease pair with a role in the DDR.
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PML degradation mechanism through Notch/Hey1-induced repression of USP11 involved in brain tumour pathogenesis
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USP11 is a novel regulator of p53, which is required for p53 activation in response to DNA damage
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Our data support a model whereby USP11 domains outside the catalytic core domain serve as protein interaction or trafficking modules rather than a direct regulatory function of the proteolytic activity.
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USP-11 is not a predictor of a pCR after anthracycline-taxane-containing NST for breast cancer. Low USP-11 expression was independently correlated with better survival outcomes.
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USP11 augments TGFbeta signalling by deubiquitylating ALK5.
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Ablation of either USP7 or USP11 in primary human fibroblasts results in de-repression of the INK4a tumour suppressor accompanied by loss of Polycomb repressive complex 1 binding at the locus and a senescence-like proliferative arrest.