Project description:The RAS pathway is frequently exploited by cancer cells to sustain their proliferation and survival. ERK is the most distal kinase in the RAS signaling cascade, playing a pivotal role in signaling output. We performed a transcriptomic analysis to obtain an overview of the consequences of EI-52 (CER) treatment, an inhibitor of ERK protein-protein interaction, on the global cellular transcriptional activity.
Project description:We examined ATF4 genomic occupancy resulting from treatment of HCT116 colon carcinoma human cell lines with DMSO, etoposide, histidinol, or, tunicamycin, using Cut&Run.
Project description:Identification of the DNA binding landscape of the transcription factor regulatory factor X 7 (RFX7) in Nutlin-3a and DMSO control treated HCT116 cells.
Project description:Axon regeneration in the central nervous system (CNS) requires reactivating injured neurons’ intrinsic growth state and enabling growth in an inhibitory environment. Using an inbred mouse neuronal phenotypic screen, we find that CAST/Ei mouse adult dorsal root ganglion neurons extend axons more on CNS myelin than the other eight strains tested, especially when pre-injured. Injury-primed CAST/Ei neurons also regenerate markedly in the spinal cord and optic nerve more than those from C57BL/6 mice and show greater spouting following ischemic stroke. Heritability estimates indicate that extended growth in CAST/Ei neurons on myelin is genetically determined, and two whole-genome expression screens yield the Activin transcript Inhba as most correlated with this ability. These screens are presented here.
Project description:Colorectal carcinoma cell line HCT116 cells were used as a model system to investigate the heterogeneity of different TP53 mutations. To this end, cells were haploidized by deleting an intronic splice site in one of the two wild-type TP53 alleles while the other copy was altered to different loss-of-function mutants via CRISPR/Cas9 gene editing. Cells expressing different haploid TP53 genotypes were treated with either Nutlin or DMSO to investigate the genetic variation between the mutants and the wild-type genotype.
Project description:overexpression of tumour suppressor ZAR1 in HCT116 (HCT116 wt and HCT116 delp53) colon carcinoma cell line (EYFPemtpy and ZAR1EYFP), sorted by Aria for fluorescent cells, RNA isolation