IndraLab

Statements

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"These results suggest that senescence compromised cancer cells expressing low levels of USP1 or treatment of cancer cells expressing high levels of USP1 with USP1 inhibitors may be more susceptible to[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In this context, FD2-Ub controls expression of pro senescence factor TAp63, and, consistently, in TAp63-dysfunctional cells, USP1 depletion failed to induce senescence (Park et al., 2013)."
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"Taken together, these data further indicate that depletion of USP1 results in increased cellular levels of FANCD2-Ub, causing increased senescence and decreased epithelial tumor growth in vivo."
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"Together, these data are consistent with the notion that senescence mediated by USP1 depletion does not produce DNA lesions that cause PCNA mono-ubiquitination."
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"Finally, we addressed the question of whether or not USP1 mediated senescence is dependent on ID HLH transcription factors."
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"Moreover, Usp1 depletion induced senescence in wild-type MEFs (XREF_FIG)."
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"Consequently, ID protein overexpression might rescue USP1 mediated senescence by suppressing CDKN1A expression."
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"Despite ectopic expression of ID1 or -2, USP1 depleted cells (shUSP1 and ID1 and shUSP1 and ID2) underwent senescence with the same kinetics as control cells depleted for USP1 alone (shC and pBABE [B0[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Together, these results show p53 and its major transcriptional target CDKN1A to be key factors required for the senescence arrest induced by USP1 depletion."
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"Usp1 depletion failed to induce senescence in the absence of TAp63, whereas Usp1 depletion in wild-type MEFs enhanced cellular senescence."
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"The RNA binding protein Hur competitively displaces 7SL to enhance p53 translation, thereby promoting cell cycle arrest and senescence.118 AS Uchl1, an lncRNA with SINEB2 repeats, enhances the expression of ubiquitin carboxyl-terminal hydrolase-1 (UCHL1) inducing senescence.119 The lncRNA-p21 through translation repressors RCK and FMRP suppresses expression of b-catenin and JunB, which are involved in cell proliferation and carcinogenesis.120 During aging various environmental stresses, telomere dysfunction and DNA damage negatively influence the cell cycle progression leading to senescence."
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"Taken together, the data demonstrate that senescence induced by USP1 depletion is associated with a persistent ATR-CHK1-p53-CDKN1A-dependent DDR, perturbed replisome dynamics, and genomic instability,[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"If an aberrant localization of FD2-Ub was indeed a gatekeeper for senescence induced by USP1 depletion, then reduced FD2 levels should mitigate the maintenance of senescence upon USP1 depletion."
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