Germline polymorphisms in genes maintaining the replication fork predict the efficacy of oxaliplatin and irinotecan in patients with metastatic colorectal cancer.
the data indicate that enhanced levels of Claspin and Timeless represent a gain of function that protects cancer cells from oncogene-induced replication stress in a checkpoint-independent manner.
ERK activation promotes TIMELESS expression in colon cancer cell lines. TIMELESS depletion increases gammaH2AX a marker of DNA damage and triggers G2/M arrest via increased CHK1 and CDK1 phosphorylation.
Results indicate a role for the DDX11-Timeless interaction in coordinating DNA replication with sister chromatid cohesion and suggest implications for understanding the molecular basis of Warsaw breakage syndrome (WABS).
we suggest that disturbances in timeless expression may result in the disruption of the control of normal circadian rhythm thus benefiting the survival of glioma cells and promoting carcinogenesis.
Results provide evidence that Timeless displays the characteristics of an ERalpha co-activator: it binds directly to ERalpha increases its transcriptional activity and is required for full ERalpha activity. This activity likely contributes to the ability of Timeless to promote breast cancer cell proliferation and may underlie the observed associations between Timeless and breast cancer patient outcome.
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