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Results suggest that CDK-mediated phosphorylation of Cdt2 inactivates its ubiquitin ligase activity by reducing its affinity to PCNA, an important strategy for regulating the levels of key proteins in the cell cycle.
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Findings suggest that DTL overexpression plays a crucial role in tumor cell proliferation in gastric carcinoma.
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CDT2 mediated XPG elimination from DNA damage sites clears the chromatin space needed for repair.
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CDT2 likely is a non-oncogene to which transformed cells become addicted because of their enhanced cellular stress, such as replicative stress and DNA damage.
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These findings reveal C/EBPalpha regulates G1/S cell cycle arrest in response to DNA damage via the control of CRL4(Cdt2) mediated degradation of p21.
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CDK1 activity blocks CRL4CDT2 by preventing chromatin recruitment of the substrate receptor, CDT2.
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while interaction with PCNA was important for targeting p21 to the CRL4Cdt2 ligase re-localized to MVM replication centers
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CRL4(Cdt2)-dependent degradation of TDG occurs in S phase because of the requirement for TDG to interact with chromatin-loaded PCNA, and this degradation is important for preventing toxicity from excess TDG.
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Data shows that phosphorylation of Cdt2 at T464 is important fot its interaction with Cdt2.
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TGF-beta signaling promotes exit from the cell cycle and cellular migration through cullin cross-regulation: SCF-FBXO11 turns off CRL4-Cdt2.
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ubiquitination of p12 through CRL4(Cdt2) and subsequent degradation form one mechanism by which a cell responds to DNA damage to inhibit fork progression.
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Data indicate that depleting ubiquitin E3 ligase CRL4(CDT2/DCAF2) mimicked the pharmacological effects of MLN4924.
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Data indicate that CRL4(Cdt2) regulates the degradation of the p12 subunit of Pol delta4.
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Non-canonical CRL4A/4B(CDT2) interacts with RAD18 to modulate post replication repair and cell survival.
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The functional interaction between FBXO11 and CDT2 is evolutionary conserved from worms to humans and plays an important role in regulating the timing of cell-cycle exit.
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Migration of epithelial cells is stimulated by CRL1(FBXO11)-mediated downregulation of Cdt2 and the consequent stabilization of Set8.
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ATR, activated after DNA damage, phosphorylates Cdt2 and promotes the rapid degradation of Cdt1 after UV irradiation in the G1 phase of the cell cycle.
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CRL4 is a major regulator of CHK1 stability. CRL4CDT2 targets CHK1 for ubiquitination in the nucleoplasm, and for PCNA-independent degradation. CHK1 is required for G2 arrest in CDT2-depleted cells.
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The turnover of SET8 is accelerated after ultraviolet irradiation dependent on the CRL4(CDT2) ubiquitin ligase and PCNA.
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data identified miR-30a-5p as a tumor-suppressing miRNA in colon cancer cells exerting its function via modulation of DTL expression, which is frequently overexpressed in colorectal cancer
