Isoginkgetin and Madrasin are poor splicing inhibitors
Michael Tellier, Gilbert Ansa, Shona Murphy
This study shows that Madrasin and Isoginkgetin inhibit transcription before affecting splicing, suggesting they are not primary splicing inhibitors.
Author
University of LeicesterORCID 0000-0002-4130-9050Unclaimed ORCID profile · follow to get notified of new preprints
9 papers
Recent·Most cited
Michael Tellier, Gilbert Ansa, Shona Murphy
This study shows that Madrasin and Isoginkgetin inhibit transcription before affecting splicing, suggesting they are not primary splicing inhibitors.
Gilbert Ansa, Shona Murphy, Michael Tellier
This study shows that SF3B1 inhibition disrupts P-TEFb recruitment to chromatin through multiple mechanisms involving nuclear export and degradation of splicing factors.
Chihiro Nakayama, Yasukazu Daigaku, Yuki Aoi…·Takayuki Nojima
This study shows that NELF-C loss disrupts Pol II transcription termination and causes transcription-replication conflicts in colorectal cancer.
Joana Wilton, Filipa Lopes de Mendonça, Isabel Pereira‐Castro…·Alexandra Moreira
This study shows that pro-inflammatory polarization and CRC cell co-culture alter 3UTR-APA and IPA in primary human macrophages, with SRSF12 playing a key role.
Callum Henfrey, Shona Murphy, Michael Tellier
The paper investigates how cytoplasmic mRNA levels are influenced by chromatin retention and RNA stability, finding that poor RNA processing leads to increased chromatin retention and shorter half-life.
Michael Tellier, Justyna Zaborowska, Jonathan Neve…·Shona Murphy
This study shows CDK9 and PP2A regulate RNA polymerase II transcription termination and RNA maturation by modulating polyadenylation and splicing factors.
Michael Tellier, Ronald Chalmers
The paper develops constitutive expression vectors to measure DNA transposition rates and correct for auto-inhibition by testing Hsmar1 transposase variants.
Michael Tellier, Ronald Chalmers
The paper investigates SETMAR's role in DNA integration and repair by analyzing cell lines with different SETMAR variants and finds that specific domains and activities are involved in these processes.
Jessica G. Hardy, Michael Tellier, Shona Murphy, Chris J. Norbury
This study shows that the RS domain of CFIm68 is critical for selecting between alternative polyadenylation sites in human cells.