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Jeremy Austin Daniel

Jeremy Austin Daniel

Associate Professor Jeremy A. Daniel leads the Chromatin Structure & Function group in the Department of Disease Biology at CPR. Dr. Daniel’s group utilizes targeted gene inactivation in mice as a physiological model together with a combination of biochemistry, flow cytometry, and proteomics to investigate how protein complexes that modify chromatin regulate genome stability and prevent lymphoid malignancy. Through initiating dedicated in-house collaborations, the group is taking full advantage of the excellence in proteomics and next-generation mass spectrometers present at CPR.

Dr. Daniel earned his PhD from the University of Virginia, did his postdoctoral work at the National Cancer Institute, within the lab of Dr. Andre Nussenzweig, and was appointed to his current post at CPR in January 2012.

Most significant publications

Dr. Daniel has made outstanding contributions across the DNA damage/epigenetics fields and has published papers in high impact journals including Cell, Science, and Nature. One paper has been cited over 250 times and another over 100 times. Dr. Daniel has worked intensively on the mechanism and function of ATM kinase activation; he showed that 3 previously proposed critical autophosphorylation sites of ATM are dispensable for ATM function in vivo, published in the Journal of Cell Biology. As a co-corresponding author with CPR affiliation, Dr. Daniel discovered that ATM kinase-dead mice are surprisingly embryonic lethal and harbor cells with increased genomic instability, also published in the Journal of Cell Biology.  The mechanism by which DNA damage activates ATM kinase activity remains an outstanding question in the field and Dr. Daniel’s contribution has led to a deeper understanding of how cells detect and respond to DNA damage.  Perhaps attracting the most attention has been Dr. Daniel's work identifying the first histone modifying complex that directly controls chromatin accessibility critical for lymphocyte rearrangements. These results established that the PTIP (gene name Paxip) component of the MLL3 (mixed-lineage leukemia 3) /MLL4 histone H3K4 methyltransferase complex promotes transcription at the immunoglobulin heavy-chain locus, which is critical during an immune response for antibody class-switching. The work was published and highlighted in Science magazine and serves the basis for some of the independent research in his group that aims to further elucidate the functional organization and targeting of the PTIP complex during antibody class-switching.

Fellowships and awards

Dr. Daniel has been successful in obtaining funding with the highly competitive NIH K99/R00 Pathway to Independence Award as well as the Swedish Research Council Project Grant for Young Scientists, both awarded in 2011. In January 2013, Dr. Daniel was awarded the prestigious Sapere Aude Research Leader grant from The Danish Council for Independent Research for his pioneering research project focusing on understanding how DNA patterns are generated and controlled during development of healthy and cancerous white blood cells. In addition, a postdoctoral fellow in the lab, Dr. Linda M. Starnes, received a three year individual postdoctoral grant from The Danish Council for Independent Research for elucidating the function of ATM kinase activity during development.

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