{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTREX1 is the major mammalian 3′→5′ DNA exonuclease that plays a pivotal role in maintaining cellular homeostasis by degrading aberrant self‐DNA. This activity prevents the accumulation of cytosolic or extranuclear DNA that would otherwise trigger inappropriate innate immune responses through sensors such as cGAS–STING, leading to excessive type I interferon production. In keeping with its central immunomodulatory function, loss‐of‐function mutations or mislocalization of TREX1 have been implicated in a spectrum of interferon‐driven autoimmune and inflammatory disorders—including Aicardi–Goutières syndrome, systemic lupus erythematosus, familial chilblain lupus, and retinal vasculopathy with cerebral leukodystrophy—and are also associated with vascular and neuroinflammatory phenotypes. Moreover, TREX1 activity is critical for the suppression of viral DNA–mediated interferon induction during infections such as HIV, thereby permitting viral replication while averting chronic innate immune activation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its immunoregulatory role, TREX1 contributes to the safeguarding of genome integrity. Under conditions of DNA damage or replication stress, TREX1 can relocate from its endoplasmic reticulum–associated resting compartment into the nucleus during S phase, where it processes single‐stranded DNA intermediates generated from aberrant replication or nuclease‐mediated cleavage events. Such processing helps to attenuate DNA damage checkpoint signalling and prevents chronic activation of the DNA damage response. In addition, interactions between TREX1 and factors involved in DNA repair—such as PARP1—and its regulation within specialized cellular environments, for example, through phase separation mechanisms, underscore its role in curtailing excess immune stimulation without compromising essential repair processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, emerging evidence reveals that TREX1 activity is integral to processes that influence genomic instability and tumor biology. In scenarios such as telomere crisis, TREX1 mediates the nucleolytic fragmentation of dicentric chromosomes, thereby contributing to phenomena like chromothripsis and kataegis. In the tumor microenvironment, modulation of TREX1—whether through microRNA‐mediated regulation or pharmacological inhibition—can alter the local inflammatory milieu by affecting the degradation of immunostimulatory DNA, opening potential avenues for cancer immunotherapy strategies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yanick J Crow, Bruce E Hayward, Rekha Parmar, et al. 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