Christopher Geoffrey Woods

The paper identifies a Kv6.4 variant that selectively reduces function without affecting other Kv6 subunits, suggesting it as a therapeutic target for uterine pain.

The paper functionally characterizes six SCN9A missense variants associated with CIP, revealing that they cause complete loss-of-function through structural changes in the extracellular vestibule, ion selectivity filter, and N-terminus.

The paper compares genetic and pharmacological loss-of-function mechanisms of Nav1.7 analgesia, highlighting distinct opioid-dependent and -independent pathways in embryonic and adult stages.

This study uses genome sequencing to identify causal variants in families with neurodevelopmental disorders, finding 36% of affected individuals have causal variants and 26% have variants of uncertain significance.

The paper analyzes X-linked coding variation in developmental disorders, finding similar rates in males and females and estimating pathogenicity of inherited variants.

The paper identifies a genetic variant in KCNG4 associated with increased labor pain by altering KV6.4 function in uterine nociceptors.