Publications by authors named "James H Hickling"
Article Synopsis
- Type III CRISPR systems protect against genetic threats by producing cyclic oligo-adenylate (cA) that activates effector proteins with CRISPR-associated Rossman fold (CARF) domains.
- Researchers studied an effector called CRISPR-associated adenosine deaminase 1 (Cad1), which converts ATP to ITP when cA binds to its CARF domain.
- Structural analysis showed Cad1 forms a hexameric assembly and, when activated by cA during a viral infection, it causes a growth arrest in the host, preventing viral replication and demonstrating diverse immune mechanisms in prokaryotes.
Chromosomal instability is a hallmark of human cancer that is associated with aggressive disease characteristics. Chromosome mis-segregations help fuel natural selection, but they risk provoking a cGAS-STING immune response through the accumulation of cytosolic DNA. The mechanisms of how tumors benefit from chromosomal instability while mitigating associated risks, such as enhanced immune surveillance, are poorly understood.
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