Background: Similar to colonic diverticula, small-intestinal diverticula are often asymptomatic, but may cause life-threatening acute complications. Non-Meckel's small-bowel diverticular perforation is rare, and the rate of mortality is high. However, there is currently no consensus regarding its therapeutic management.
View Article and Find Full Text PDFCellular senescence plays a causal role in ageing and, in mice, depletion of p16-expressing senescent cells delays ageing-associated disorders. Adenosine deaminases acting on RNA (ADARs) are RNA-editing enzymes that are also implicated as important regulators of human ageing, and ADAR inactivation causes age-associated pathologies such as neurodegeneration in model organisms. However, the role, if any, of ADARs in cellular senescence is unknown.
View Article and Find Full Text PDFAdenosine deaminase acting on RNA (ADAR) catalyzes the posttranscriptional conversion of adenosine to inosine in double-stranded RNA (dsRNA), which can lead to the creation of missense mutations in coding sequences. Recent studies show that editing-dependent functions of ADAR1 protect dsRNA from dsRNA-sensing molecules and inhibit innate immunity and the interferon-mediated response. Deficiency in these ADAR1 functions underlie the pathogenesis of autoinflammatory diseases such as the type I interferonopathies Aicardi-Goutieres syndrome and dyschromatosis symmetrica hereditaria.
View Article and Find Full Text PDFADAR1 is involved in adenosine-to-inosine RNA editing. The cytoplasmic ADAR1p150 edits 3'UTR double-stranded RNAs and thereby suppresses induction of interferons. Loss of this ADAR1p150 function underlies the embryonic lethality of Adar1 null mice, pathogenesis of the severe autoimmune disease Aicardi-Goutières syndrome, and the resistance developed in cancers to immune checkpoint blockade.
View Article and Find Full Text PDF