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Articles by Elias Einig
RNAPII-dependent ATM signaling at collisions with replication forks - Nature Communications
Abstract Deregulation of RNA Polymerase II (RNAPII) by oncogenic signaling leads to collisions of RNAPII with DNA synthesis machinery (transcription-replication conflicts, TRCs). TRCs can result in DNA damage and are thought to underlie genomic instability in tumor cells. Here we provide evidence that elongating RNAPII nucleates activation of the ATM kinase at TRCs to stimulate DNA repair. We show the ATPase WRNIP1 associates with RNAPII and limits ATM activation during unperturbed cell cycle.
Trim33 masks a non-transcriptional function of E2f4 in replication fork progression - Nature Communications
Abstract Replicative stress promotes genomic instability and tumorigenesis but also presents an effective therapeutic endpoint, rationalizing detailed analysis of pathways that control DNA replication. We show here that the transcription factor E2f4 recruits the DNA helicase Recql to facilitate progression of DNA replication forks upon drug- or oncogene-induced replicative stress.
USP28 controls SREBP2 and the mevalonate pathway to drive tumour growth in squamous cancer - Cell Death & Differentiation
Tissue culture and reagents Cell lines were obtained from ATCC (American Type Culture Collection, Chicago, IL, USA) and used at low passage. Cells were cultured in DMEM (A431, U2OS, HEK293T) or RPMI 1640 (NCI-H520, LUDLU1, CALU-1, NCI-H522, NCI-H1299, A549) supplemented with 10% foetal calf serum (FCS), 2 mmol/L glutamine and 100 U/mL penicillin/streptomycin (all Sigma). Delipidated FCS was prepared as previously described [23].
LXRα activation and Raf inhibition trigger lethal lipotoxicity in liver cancer - Nature Cancer
Abstract The success of molecular therapies targeting specific metabolic pathways in cancer is often limited by the plasticity and adaptability of metabolic networks. Here we show that pharmacologically induced lipotoxicity represents a promising therapeutic strategy for the treatment of hepatocellular carcinoma (HCC). LXRα-induced liponeogenesis and Raf-1 inhibition are synthetic lethal in HCC owing to a toxic accumulation of saturated fatty acids.
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