Clinical heterogeneity among a three-generation Japanese family with D18N TREX1 mutation for Aicardi-Goutières syndrome / familial chilblain lupus

نویسندگان

  • J Abe
  • R Nishikomori
  • K Izawa
  • T Awaya
  • T Kawai
  • T Yasumi
  • T Heike
  • N Hiragi
  • T Hiragi
چکیده

Background Aicardi-Goutières syndrome (AGS) is a genetic disease, characterized by encephalopathy with cerebral calcification, white matter abnormalities, cerebral atrophy, elevated interferon-alpha in the cerebrospinal fluid and chilblain. Most of AGS patients have severe neurological findings including developmental delay. Five genes, namely TREX1, RNASEH2B, RNASEH2C, RNASEH2A, SAMHD1 have been reported to be responsible for AGS. Most cases of AGS are inherited as autosomal recessive manner, although autosomal dominant AGS is rarely reported and its clinical manifestations are largely unknown.

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Aicardi–Goutières syndrome protein TREX1 suppresses L1 and maintains genome integrity through exonuclease-independent ORF1p depletion

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RAPID COMMUNICATIONS A mutation in TREX1 that impairs susceptibility to granzyme A-mediated cell death underlies familial chilblain lupus

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عنوان ژورنال:

دوره 9  شماره 

صفحات  -

تاریخ انتشار 2011