Michael T. Howell

This study identifies distinct roles of ATRX in safeguarding genome and telomere integrity through interactions with CST and 9-1-1 complexes, revealing context-dependent mechanisms.

This study identifies relapse-founding cancer persister cells in follicular lymphoma using a mouse model and shows their transcriptional program is conserved in humans, with potential therapeutic targets identified.

The paper identifies a covalent fragment inhibitor of TYMS that selectively kills ATRX-deficient cells through replication stress.

The paper uses genomic barcoding and single-cell RNA sequencing to reveal hierarchical lineage architecture in human and avian spinal cord development, showing conserved lineage restriction and developmental routes.

The paper uses a CRISPR-Cas9 screen to identify host genes critical for Cryptosporidium survival, revealing a metabolic dependency on host cholesterol biosynthesis that can be targeted for treatment.

This study identifies a global temporal chromatin programme in vertebrate neural progenitors that integrates with spatial patterning to regulate cell fate and identity.

This study identifies how the DNA damage checkpoint stabilizes replication forks by preventing excess origin firing and fork collapse through the regulation of PCNA and HLTF.

This study shows SARS-CoV-2 E protein induces LC3 lipidation through the V-ATPase-ATG16L1 axis, which supports viral replication rather than inhibiting it.

This study identifies vinorelbine as a compound that enhances the efficacy of a GM-CSF-armed oncolytic vaccinia virus in treating ovarian cancer in mice.

This paper introduces asymmetric contrastive objectives for phenotypic screening, improving performance on benchmark datasets and real-world cell screening tasks.

The paper functionally profiles long intergenic non-coding RNAs (lincRNAs) in fission yeast by analyzing mutant phenotypes across various conditions.

This study identifies inherited PPP2R3B duplications as a melanoma predisposing factor, revealing a C21orf91-driven proliferative phenotype in melanocytes.

This study identifies mechanisms regulating YAP1 nuclear shuttling in fibroblasts, showing that Src and actomyosin suppress YAP1 export, and nuclear export is central to YAP1 regulation.