Seth M. Rubin

THE FAM53C/DYRK1A axis regulates the G1/S transition of the cell cycle

This study identifies FAM53C as a regulator of the G1/S cell cycle transition, showing it interacts with DYRK1A and affects cell cycle progression in cultured cells and organoids.

A Fkh1/2 binding site array in the WHI5 promoter drives sub-scaling transcription

E2F1 induces a G0-G1 reentry transcriptional program without changing chromatin accessibility

The paper shows E2F1 induces cell-cycle reentry without changing chromatin accessibility by using pre-existing regulatory elements.

Tandem association of CLOCK:BMAL1 complexes on DNA enables recruitment of CBP/p300 through multivalent interactions

The paper shows that tandem E-boxes enable CLOCK:BMAL1 to bind more sites on nucleosomes, promoting multivalent interactions with CBP/p300 to drive gene expression.

Structural mechanism for recognition of E2F1 by the ubiquitin ligase adaptor Cyclin F

The paper determines the structure of Cyclin F-Skp1 complex bound to E2F1 peptide, revealing differences in substrate-binding site and electrostatic interactions compared to Cyclin A.

Structural and functional analysis of cancer-associated missense variants in the retinoblastoma protein (Rb) pocket domain

This study analyzes how cancer-associated missense variants in Rb's pocket domain affect its binding and stability using biophysical assays and crystallography.

HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes

This study shows that DREAM and E2F:RB complexes can repress cell-cycle genes without HDAC activity, challenging the canonical role of HDACs in this process.

The MuvB Complex Binds and Stabilizes Nucleosomes Downstream of the Transcription Start Site of Cell-Cycle Dependent Genes

This study determines the structure of the MuvB complex and shows it binds and stabilizes nucleosomes downstream of the transcription start site to repress gene expression.

A Long Lost Key Opens an Ancient Lock: Drosophila Myb Causes a Synthetic Multivulval Phenotype in Nematodes

This paper shows that Drosophila Myb can bind to nematode LIN9 and LIN52 proteins and cause a synthetic multivulval phenotype in C. elegans, despite their distant evolutionary divergence.