Unknown,Transcriptomics,Genomics,Proteomics

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RNA-SEQ analysis of KMC murine pancreatic ductal adenocarcinoma (PDAC) cell line upon siRNA depletion of MYC, KRas or Miz1 (aka Zbtb17)


ABSTRACT: MYC is varyingly thought to either complement KRAS or to act as a downstream KRAS effector - here we compared the transcriptomic impact of MYC depletion with that of KRas depletion in a cell line derived from PDAC driven by lsl-KRas^G12D + Rosa26-lsl-MYC^DM. A second question addressed related to the mechanism of MYC-dependent transcriptional repression, which in many instances requires MYC binding to Miz1. We therefore included analysis of Miz1-depleted KMC cells in this experiment

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Daniel Murphy 

PROVIDER: E-MTAB-8792 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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