Bastien Morlet

This study shows Pho92 interacts with Not1 to recruit the CCR4-NOT complex to m6A-containing mRNAs, modulating meiosis in S. cerevisiae.

The paper reports a large-scale quantitative interactome of human PDZ domains and bacterial PDZ-binding motifs, showing bacteria tailor effector sequences to bind with similar or higher affinity than human PBMs to hijack host functions.

This study shows that glucocorticoid receptor signaling in myeloid cells affects inflammation resolution and muscle repair by regulating macrophage dynamics and satellite cell function.

This study quantifies how mutations in GATA1 affect DNA binding affinity using a new assay, revealing that certain mutations reduce binding while others increase it.

The paper identifies a human-specific TAF8 isoform arising from an Alu insertion that alters TFIID complex composition and function.

The paper identifies CHD1L as a key regulator of neurodevelopmental processes, showing its role in shaping neuroanatomical and growth phenotypes linked to 1q21.1 copy number variants.

This study shows that partially assembled TFIID complexes can initiate RNA polymerase II transcription but cannot fully replace holo-TFIID over time.

The paper identifies functional differences in PDZ-binding motifs among DGK enzyme types using interactomic and evolutionary analyses.

This study shows that ATAC and SAGA coactivator complexes assemble co-translationally in the cytoplasm, but their localization and functions differ.

The paper identifies HELZ2, a new human RNB family protein expressed from a non-canonical initiation codon, which functions as an interferon-regulated 3'-5' exoribonuclease with RNA degradation activity.

This study identifies a noncanonical role of Kif21b in regulating actin cytoskeleton dynamics during radial migration of cortical projection neurons in mice.

The paper shows TFIID biogenesis occurs co-translationally through hierarchical assembly driven by TAF1.

The paper introduces nHU, a method to quantify binding affinities from cell extracts, showing agreement between in vitro and in-cell measurements.

The paper measures affinities of 65,000 PDZ domain interactions using quantitative fragmentomics, revealing viral interference hotspots and system-wide impacts of interactome hijacking.

This study shows that SUPT3H is not essential for SAGA complex assembly or overall Pol II transcription but is required for mESC growth and self-renewal.