Carl R. Walkley

Minute amounts of helicase-deficient truncated RECQL4 are sufficient for DNA replication.

This study identifies KLHDC3 as a rescue factor for RECQL4 mutations, showing that low levels of a truncated RECQL4 protein can support DNA replication without requiring its ATPase or helicase domains.

ADAR1p150 RNA binding, independent of A-to-I RNA editing, buffers immunogenicity from the tonic type I IFN induced transcriptome in vivo.

This study shows ADAR1p150 suppresses immunogenicity from tonic type I IFN-induced transcripts through editing-dependent and -independent mechanisms.

Deletion of KLHDC3, an E3 ubiquitin ligase complex substrate receptor, leads to obesity in mice.

This study shows that deleting Klhdc3 in mice causes obesity and developmental issues, highlighting its role in regulating protein stability and adiposity.

Genome-Wide CRISPR-Cas9 Screening Identifies a Synergy between Hypomethylating Agents and SUMOylation Blockade in MDS/AML

This study identifies a synergy between hypomethylating agents and SUMOylation blockade in MDS/AML using CRISPR-Cas9 screening, showing improved therapeutic outcomes in xenograft models.

ADAR1p150 Prevents MDA5 and PKR Activation via Distinct Mechanisms to Avert Fatal Autoinflammation

The paper shows that ADAR1p150 prevents MDA5 and PKR activation through distinct mechanisms, preventing fatal autoinflammation.

Generation of a new Adar1p150-/- mouse demonstrates isoform-specific roles in embryonic development and adult homeostasis.

This paper generates and characterizes a new Adar1p150-/- mouse model, showing its essential role in embryonic development and adult homeostasis through IFN response suppression.

The most common human ADAR1p150 Zα domain mutation P193A is well tolerated in mice.

The paper reports that the common ADAR1p150 mutation P193A is well tolerated in mice, with reduced severity when combined with MDA5 loss.

Dynamic DNA structure states interact with the RNA editing enzyme ADAR1 to modulate fear extinction memory

This study shows ADAR1 interacts with Z-DNA during fear extinction learning, affecting RNA editing and memory flexibility.