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UID:DSC-21625
DTSTART;TZID=Europe/Berlin:20250828T130000
SEQUENCE:1756359494
TRANSP:OPAQUE
DTEND;TZID=Europe/Berlin:20250828T140000
URL:https://www.dresden-science-calendar.de/calendar/en/detail/21625
LOCATION:TUD CRTD\, Fetscherstraße 10501307 Dresden
SUMMARY:CMCB Life Sciences Seminar: Dr. Yuval Dor\, The Hebrew University o
 f Jerusalem\, Faculty of Medicine\, Israel
CLASS:PUBLIC
DESCRIPTION:Speaker: \nInstitute of Speaker: \nTopics:\nBiologie\, Willkomm
 en\n Location:\n  Name: TUD CRTD ()\n  Street: Fetscherstraße 105\n  City
 : 01307 Dresden\n  Phone: +49 (0)351 458 82052\n  Fax: +49 (0)351 458 8205
 9 \nDescription: <p><strong>Hosts:</strong> Karsten Kretschmer &amp\; Niko
 lay Ninov (CRTD)</p> <p><strong>Title:</strong> “Impaired RNA editing as
  a path to islet inflammation and diabetes”</p> <p><strong>Abstract:</st
 rong> A major hypothesis for the etiology of type 1 diabetes (T1D) postula
 tes initiation by viral infection\, leading to double-stranded RNA (dsRNA)
 -mediated interferon response and inflammation\; however\, a causal virus 
 has not been identified. We have used a mouse model\, corroborated with hu
 man islet data\, to demonstrate that endogenous dsRNA in beta cells can le
 ad to a diabetogenic immune response\, thus identifying a virus-independen
 t mechanism for T1D initiation. We found that disruption of the RNA editin
 g enzyme ADAR in beta cells triggers a massive interferon response\, islet
  inflammation and beta cell failure and destruction\, with features bearin
 g striking similarity to early-stage human T1D. Glycolysis via calcium enh
 ances the interferon response\, suggesting an actionable vicious cycle of 
 inflammation and increased beta cell workload. Thus\, defects in RNA editi
 ng in beta cell may lead to the accumulation of endogenous dsRNA and to is
 let inflammation and diabetes. I will present published and unpublished da
 ta supporting the hypothesis that defects in RNA editing may contribute to
  early stages of T1D\, and shed light on unexplained T1D phenomena.</p>
DTSTAMP:20260509T221343Z
CREATED:20250110T063913Z
LAST-MODIFIED:20250828T053814Z
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