Publications by authors named "Jacob M Gross"

DNA methylation is a key regulator of gene expression and a clinical therapeutic predictor. We examined global DNA methylation beyond the generally used promoter areas in human small cell lung cancer (SCLC) and find that gene body methylation is a robust positive predictor of gene expression. Combining promoter and gene body methylation better predicts gene expression than promoter methylation alone including genes involved in the neuroendocrine classification of SCLC and the expression of therapeutically relevant genes including , and .

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During routine genome duplication, many potential replication origins remain inactive or 'dormant'. Such origin dormancy is achieved, in part, by an interaction with the metabolic sensor SIRT1 deacetylase. We report here that dormant origins are a group of consistent, pre-determined genomic sequences that are distinguished from baseline (i.

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Safeguards against excess DNA replication are often dysregulated in cancer, and driving cancer cells towards over-replication is a promising therapeutic strategy. We determined DNA synthesis patterns in cancer cells undergoing partial genome re-replication due to perturbed regulatory interactions (re-replicating cells). These cells exhibited slow replication, increased frequency of replication initiation events, and a skewed initiation pattern that preferentially reactivated early-replicating origins.

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Background: Next-generation sequencing allows genome-wide analysis of changes in chromatin states and gene expression. Data analysis of these increasingly used methods either requires multiple analysis steps, or extensive computational time. We sought to develop a tool for rapid quantification of sequencing peaks from diverse experimental sources and an efficient method to produce coverage tracks for accurate visualization that can be intuitively displayed and interpreted by experimentalists with minimal bioinformatics background.

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Article Synopsis
  • - The spindle assembly checkpoint (SAC) delays chromosome separation until all chromosomes are properly attached, guarding against errors during cell division by inactivating the APC/C complex.
  • - The study highlights the role of the CRL4 complex, which, during mitosis, helps end the SAC and allows for chromosome segregation by replacing RepID with RBBP7, leading to the degradation of the SAC mediator BUB3.
  • - Deficiencies in RepID, CRL4, or RBBP7 can cause delays in mitotic exit, increased genomic instability, and heightened sensitivity to paclitaxel, which is used in cancer treatment.
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