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To find putative mechanisms of drug resistance in cancers with BRAF mutations, we initially identified medicines active in most cancers cell traces with BRAF missense mutations using the from gene to drug

Dysregulated DnaB unwinding induces replisome decoupling and daughter strand gaps which might be countered by RecA polymerization PHF2 regulates genome topology and DNA replication click here in neural stem cells by means of cohesin LowTempGAL: a very responsive minimal temperature-inducible GAL

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Right here, we will briefly current how GDA can combine drug responses, mutations, and gene expression profiles to formulate hypotheses around the mechanisms linked to drug resistance or to elucidate the interaction amongst the transcriptional activation of signaling pathways and drug response.

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