A. N. Kettenbach

This study identifies brd-8 as a circadian-regulated component of the NuA4 histone acetyltransferase complex that modulates frq expression and circadian rhythm in Neurospora.

The paper uses proteomics and phosphoproteomics to analyze PPP2R5D variants, finding RPS6 hyperphosphorylation and mTORC1 activation through different pathways in E198K and E420K variants.

The paper uses inducible protein degradation to identify Phosphoprotein Phosphatase 6 substrates in RAS-mutant colorectal cancer cells and reveals its role in mitotic regulation.

This study identifies phosphoprotein phosphatase activity as a positive regulator of oligomeric pyrin, essential for inflammasome assembly in phagocytes.

The paper shows that positive feedback in the β-catenin destruction complex creates bistability and memory in Wnt signaling, leading to switch-like cellular responses.

This study investigates how C-terminal methylation regulates PP2A, PP4, and PP6 holoenzyme assembly using proteomics and genetic approaches, revealing methylation-dependent interactions in cancer and non-transformed cells.

This study identifies Ssn3 kinase substrates involved in hyphal growth repression through Flo8 phosphorylation in C. albicans.

This study identifies a conserved SLiM in p107 that mediates B55 recruitment and dephosphorylation, revealing a general mechanism for PP2A/B55 substrate recognition.

The paper identifies PP2A-B55's role in meiosis I to II transition through selective dephosphorylation of threonine residues in sea star oocytes.

This study identifies Pak1 as a kinase that phosphorylates Mid1 to regulate cytokinesis in fission yeast by controlling CAR assembly and division plane positioning.

This study identifies STK32A as a dual-specificity AGC kinase preferring acidic substrates, revealing structural and evolutionary features supporting its substrate specificity.

This study identifies how Cdr1/Nim1 kinase inhibits Wee1 to promote mitotic entry by phosphorylating specific serine residues in yeast.

The paper identifies a complex of lysine-acetylated actin and CAP as an inhibitor of INF2, revealing a novel mechanism of facilitated auto-inhibition linked to disease.