CORDIS Project
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This project investigates the role of the ATMIN protein in activating the ATM protein kinase, particularly under conditions of hypotonic stress. It aims to understand the molecular mechanisms of ATM signaling independent of DNA damage, which is crucial for immune function and cancer prevention in B cells.
ATM is the protein kinase that is mutated in the hereditary autosomal recessive disease ataxia telangiectasia (A-T). A-T patients display immune deficiencies, cancer predisposition and radiosensitivity.
The molecular role of ATM is to respond to DNA damage by phosphorylating its substrates, thereby promoting repair of damage or arresting the cell cycle.
Following the induction of double-strand breaks (DSBs), the NBS1 protein is required for activation of ATM.
But ATM can also be activated in the…
THE FRANCIS CRICK INSTITUTE LIMITED
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