Publications by authors named "G P Oakley"

The ATR kinase responds to elevated levels of single-stranded DNA (ssDNA) to activate the G2/M checkpoint, regulate origin utilization, preserve fork stability, and allow DNA repair to ensure genome integrity. The intrinsic replication stress in cancer cells makes this pathway an attractive therapeutic target. The ssDNA that drives ATR signaling is sensed by the ssDNA-binding protein replication protein A (RPA), which acts as a platform for ATRIP recruitment and subsequent ATR activation by TopBP1.

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The ATR kinase responds to elevated levels of single-stranded DNA (ssDNA) to activate the G2/M checkpoint, regulate origin utilization, preserve fork stability, and allow DNA repair towards ensuring genome integrity. The intrinsic replication stress in cancer cells makes this pathway an attractive therapeutic target. The ssDNA that drives ATR signaling is sensed by the ssDNA-binding protein replication protein A (RPA), which acts as a platform for ATRIP recruitment and subsequent ATR activation by TopBP1.

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Article Synopsis
  • Telangiectases and arteriovenous malformations (AVMs) are key features of Hereditary Hemorrhagic Telangiectasia (HHT), linked to genetic mutations in specific HHT-related genes.
  • Researchers analyzed DNA from various tissue samples from individuals with HHT to understand the genetic mechanisms behind AVM formation and found somatic second-hit mutations contributing to these lesions.
  • This study is the first to demonstrate that both nasal telangiectasias and solid organ AVMs in HHT are associated with low-level somatic biallelic second-hit mutations, highlighting the complexity of HHT's genetic landscape.*
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The analysis of histopathology images with artificial intelligence aims to enable clinical decision support systems and precision medicine. The success of such applications depends on the ability to model the diverse patterns observed in pathology images. To this end, we present Virchow, the largest foundation model for computational pathology to date.

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