James M. Murphy

This study identifies dysregulated epithelial cell death signaling in inflammatory bowel disease, showing it persists during remission despite therapy.

This study shows that necroptosis in keratinocytes promotes differentiation and slows wound healing by preserving barrier integrity, suggesting it can be modulated to enhance tissue repair.

This study identifies SMCHD1 as a target for gene-activation therapy in Prader-Willi Syndrome by showing its role in repressing the PWS gene cluster and demonstrating gene activation in mouse models.

This study identifies a second DNA-binding site in SMCHD1 and shows that DNA binding stimulates its ATPase activity, revealing a mechanism for gene silencing.

This study compares three RIPK3 kinase-dead variants to show that their scaffolding functions differ based on kinase domain conformation, not just kinase activity, and highlights implications for inhibitor development.

The paper identifies an unconventional mechanism where Ca2+-CaM binds CHK2 kinase to inhibit its activity, contrasting with its typical role in promoting kinase activity.

This paper uses lipid nanoparticles to deliver mRNA encoding intrabodies that inhibit necroptosis and pyroptosis by targeting MLKL and ASC, respectively.

This study shows that partial reduction of BECLIN1 in intestinal epithelial cells leads to intestinal defects and increased susceptibility to inflammation, suggesting its importance in maintaining gut health.

The paper identifies allosteric regulation of PSKH1 kinase activity by Ca2+ sensor proteins, showing both activation and suppression by different sensors.

The paper develops automated immunohistochemistry protocols to detect necroptotic pathway proteins in mouse and human tissues, revealing heterogeneity and disease-related changes in expression.

This study identifies a mutation in SMCHD1 that enhances gene silencing and disrupts developmental processes, revealing distinct roles of SMCHD1 in chromatin structure and gene regulation.

This study demonstrates that MLKL ubiquitylation, triggered by oligomerization, regulates necroptosis by modulating MLKL activity and turnover.

This study elucidates how NanR represses sialic acid metabolism in E. coli by showing its cooperative DNA binding and allosteric regulation by N-acetylneuraminate.

This study identifies Smchd1 as a regulator of long-range chromatin interactions, showing context-dependent effects on transcription and chromatin structure.