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article, lupus, google, scholar, pubmed, cas, trex, erythematosus, familial, chilblain, systemic, dna, syndrome, mutation, granzyme, cell, aicardigoutieres, perrino, genet, privacy, cookies, content, journal, research, death, leekirsch, lieberman, access, publish, search, amediated, chowdhury, harvey, hubner, encoding, exonuclease, robins, lindahl, nat, neuropediatrics, biol, dresden, personal, data, information, log, molecular, medicine, april, min,

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min ae lee-kirsch month download article/chapter gene-targeted mice lacking familial chilblain lupus article lee-kirsch systemic lupus erythematosus chilblain lupus erythematosus dominant aicardi-goutieres syndrome perrino max-delbrück-center aicardi-goutieres syndrome-report related subjects cutaneous lupus erythematosus cutaneous lupus erythematosus 3′-5′repair exonuclease 1 full article pdf progressive familial encephalopathy cell tolerance checkpoints gene encoding privacy choices/manage cookies aicardi-goutieres syndrome norbert hubner chilblain lupus crow yj caspase-independent nuclease lupus erythematosus caspase-independent form autosomal-dominant genodermatosis chronic polyarthritis caused 1982 revised criteria check access instant access heterozygous missense mutation pro-resolving concept black dn cerebral thrombotic microangiopathy beresford pj angela rösen-wolff harvard medical school robert-rössle-str mammalian dna conditions privacy policy maoliang gong european economic area abundant intracellular dnase lymphoblastoid cells carrying martinez-frias ml dnase1-deficient mice article journal molecular medicine aims books a

Questions {❓}

• Aicardi J, Goutieres F (2000) Systemic lupus erythematosus or Aicardi-Goutieres syndrome?

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         headline:A mutation in TREX1 that impairs susceptibility to granzyme A-mediated cell death underlies familial chilblain lupus
         description:We recently described a novel autosomal-dominant genodermatosis, termed familial chilblain lupus, and mapped its genetic locus to chromosome 3p21. Familial chilblain lupus manifests in early childhood with ulcerating acral skin lesions and is associated with arthralgias and circulating antinuclear antibodies. In this study, we report the identification of a heterozygous missense mutation (D18N) in TREX1 encoding the 3′-5′repair exonuclease 1 in affected individuals of the family with chilblain lupus. The homodimeric TREX1 is the most abundant intracellular DNase in mammalian cells. We have recently shown that TREX1 plays a role in apoptotic single-stranded DNA damage induced by the killer lymphocyte protease granzyme A. D18N affects a highly conserved amino acid residue critical for catalytic activity. Recombinant mutant TREX1 homodimers are enzymatically inactive, while wild type/mutant heterodimers show residual exonucleolytic activity, suggesting a heterozygous loss of function. Lymphoblastoid cells carrying the D18N mutation are significantly less sensitive to granzyme A-mediated cell death, suggesting a novel role for this caspase-independent form of apoptosis in the pathogenesis of familial chilblain lupus. Our findings also warrant further investigation of TREX1 in common forms of lupus erythematosus.
         datePublished:2007-04-18T00:00:00Z
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            Autoimmune disease
            Molecular Medicine
            Human Genetics
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      headline:A mutation in TREX1 that impairs susceptibility to granzyme A-mediated cell death underlies familial chilblain lupus
      description:We recently described a novel autosomal-dominant genodermatosis, termed familial chilblain lupus, and mapped its genetic locus to chromosome 3p21. Familial chilblain lupus manifests in early childhood with ulcerating acral skin lesions and is associated with arthralgias and circulating antinuclear antibodies. In this study, we report the identification of a heterozygous missense mutation (D18N) in TREX1 encoding the 3′-5′repair exonuclease 1 in affected individuals of the family with chilblain lupus. The homodimeric TREX1 is the most abundant intracellular DNase in mammalian cells. We have recently shown that TREX1 plays a role in apoptotic single-stranded DNA damage induced by the killer lymphocyte protease granzyme A. D18N affects a highly conserved amino acid residue critical for catalytic activity. Recombinant mutant TREX1 homodimers are enzymatically inactive, while wild type/mutant heterodimers show residual exonucleolytic activity, suggesting a heterozygous loss of function. Lymphoblastoid cells carrying the D18N mutation are significantly less sensitive to granzyme A-mediated cell death, suggesting a novel role for this caspase-independent form of apoptosis in the pathogenesis of familial chilblain lupus. Our findings also warrant further investigation of TREX1 in common forms of lupus erythematosus.
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         Systemic lupus erythematosus
         TREX1
         Genetics
         Apoptosis
         Autoimmune disease
         Molecular Medicine
         Human Genetics
         Internal Medicine
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