Robert K. Bradley

A U1-U3 snRNA-snoRNA interaction couples SF3B1 mutation to chromatin-state rewiring and genome instability

This paper identifies a U1-U3 snRNA-snoRNA interaction that links SF3B1 mutations to chromatin-state changes and genome instability, with therapeutic potential through antisense oligonucleotides.

Generative genomics accurately predicts future experimental results

This paper introduces GEM-1, a generative model that accurately predicts future gene expression experiments, achieving performance comparable to real lab experiments.

Chorionic Gonadotropin Beta 7 is a marker of immune evasion in cancer

The paper identifies CGB7 as a marker of immune evasion in cancer, associated with poor prognosis and resistance to immune checkpoint inhibitor therapy.

RBM10 loss induces aberrant splicing of cytoskeletal and extracellular matrix mRNAs and promotes metastatic fitness.

This study shows that RBM10 loss causes aberrant splicing of cytoskeletal and ECM genes, leading to RAC1 activation and metastatic fitness in thyroid cancer.

Recursive splicing discovery using lariats in total RNA sequencing

This study identifies recursive splice sites in human introns using intron lariats, showing their prevalence and role in alternative exon exclusion across vertebrates.

Nonsense-mediated mRNA decay utilizes complementary mechanisms to suppress mRNA and protein accumulation

The paper quantifies mRNA and protein levels using a reporter system to show NMD suppresses protein accumulation more than mRNA.

Discovery of synthetic lethal and tumor suppressive paralog pairs in the human genome

The paper identifies synthetic lethal and tumor suppressive paralog pairs in the human genome using a CRISPR-based approach, revealing new drug targets and essential gene families.

RNA components of the spliceosome regulate tissue- and cancer-specific alternative splicing

This study shows that spliceosome RNA components regulate tissue- and cancer-specific alternative splicing by modulating splice site choice and gene expression in breast cancer.

Quantitative proteomics reveals key roles for post-transcriptional gene regulation in the molecular pathology of FSHD

The paper quantifies proteomic changes in DUX4-expressing cells, revealing post-transcriptional dysregulation in FSHD pathology.

Translational plasticity facilitates the accumulation of nonsense genetic variants in the human population

The paper shows common nonsense genetic variants are tolerated due to translational plasticity mechanisms that preserve protein function.