Matches in SemOpenAlex for { <https://semopenalex.org/work/W2102424853> ?p ?o ?g. }
- W2102424853 endingPage "1588" @default.
- W2102424853 startingPage "1580" @default.
- W2102424853 abstract "Polymorphisms in <i>NOD2</i>, encoding an intracellular pattern recognition receptor, contribute the largest fraction of genetic risk for Crohn9s disease among the >40 risk loci identified so far. Autophagy plays a prominent role in the innate immune response towards intracellular bacteria. The discovery of the autophagy genes <i>ATG16L1</i> and <i>IRGM</i> as risk factors for Crohn9s disease turned autophagy into the spotlight in inflammatory bowel disease (IBD). Remarkably, NOD2 has recently been identified as a potent autophagy inducer. A physical interaction of NOD2 and ATG16L1 appears to be required for autophagic clearance of intracellular pathogens. Moreover, Crohn9s disease-associated NOD2 and ATG16L1 variants exhibit a defect in the induction of an autophagic response and hence predict autophagy as a key converging mechanism that leads to Crohn9s disease. Another pathway that is closely intertwined with autophagy and mutually cross-regulated is the unfolded protein response (UPR), which is induced by endoplasmic reticulum (ER) stress. Genes involved in the UPR (<i>XBP1, ORMDL3</i>) have also been genetically associated with Crohn9s disease and ulcerative colitis. Moreover, the intestinal epithelium at the interface between host and microbe appears particularly affected by IBD-associated hypomorphic function of autophagy and the UPR. The functional convergence of main genetic risk factors for IBD on these innate immune pathways has hence important implications for the host9s interaction with the microbiota. Moreover, the genetic convergence on these molecular mechanisms may open novel therapeutic options for IBD that deserve further exploration." @default.
- W2102424853 created "2016-06-24" @default.
- W2102424853 creator A5021999321 @default.
- W2102424853 creator A5036264788 @default.
- W2102424853 creator A5040361804 @default.
- W2102424853 creator A5050963621 @default.
- W2102424853 creator A5054599656 @default.
- W2102424853 date "2011-01-19" @default.
- W2102424853 modified "2023-10-05" @default.
- W2102424853 title "Crohn's disease: NOD2, autophagy and ER stress converge" @default.
- W2102424853 cites W1642457845 @default.
- W2102424853 cites W1670573097 @default.
- W2102424853 cites W1808736595 @default.
- W2102424853 cites W1966860807 @default.
- W2102424853 cites W1970101770 @default.
- W2102424853 cites W1971046821 @default.
- W2102424853 cites W1973785682 @default.
- W2102424853 cites W1976531450 @default.
- W2102424853 cites W1979859398 @default.
- W2102424853 cites W1980942517 @default.
- W2102424853 cites W1990215850 @default.
- W2102424853 cites W1991075835 @default.
- W2102424853 cites W1993688639 @default.
- W2102424853 cites W1993908556 @default.
- W2102424853 cites W2000187136 @default.
- W2102424853 cites W2001712980 @default.
- W2102424853 cites W2002636911 @default.
- W2102424853 cites W2005727437 @default.
- W2102424853 cites W2007078899 @default.
- W2102424853 cites W2007743440 @default.
- W2102424853 cites W2009706335 @default.
- W2102424853 cites W2011197968 @default.
- W2102424853 cites W2012451546 @default.
- W2102424853 cites W2013494956 @default.
- W2102424853 cites W2014475853 @default.
- W2102424853 cites W2017018900 @default.
- W2102424853 cites W2018542503 @default.
- W2102424853 cites W2021839438 @default.
- W2102424853 cites W2031558979 @default.
- W2102424853 cites W2035145212 @default.
- W2102424853 cites W2042260827 @default.
- W2102424853 cites W2043667001 @default.
- W2102424853 cites W2045743590 @default.
- W2102424853 cites W2048456744 @default.
- W2102424853 cites W2049309853 @default.
- W2102424853 cites W2049991946 @default.
- W2102424853 cites W2052127995 @default.
- W2102424853 cites W2055292040 @default.
- W2102424853 cites W2058627896 @default.
- W2102424853 cites W2059867286 @default.
- W2102424853 cites W2060643376 @default.
- W2102424853 cites W2063229389 @default.
- W2102424853 cites W2064027072 @default.
- W2102424853 cites W2064741210 @default.
- W2102424853 cites W2070405472 @default.
- W2102424853 cites W2073731887 @default.
- W2102424853 cites W2074911710 @default.
- W2102424853 cites W2077861414 @default.
- W2102424853 cites W2080100430 @default.
- W2102424853 cites W2083075230 @default.
- W2102424853 cites W2084518640 @default.
- W2102424853 cites W2084708009 @default.
- W2102424853 cites W2091608255 @default.
- W2102424853 cites W2092956992 @default.
- W2102424853 cites W2094898345 @default.
- W2102424853 cites W2095593278 @default.
- W2102424853 cites W2096308078 @default.
- W2102424853 cites W2096853390 @default.
- W2102424853 cites W2097121808 @default.
- W2102424853 cites W2097345042 @default.
- W2102424853 cites W2097875133 @default.
- W2102424853 cites W2098985594 @default.
- W2102424853 cites W2099662390 @default.
- W2102424853 cites W2100443415 @default.
- W2102424853 cites W2104722369 @default.
- W2102424853 cites W2104932289 @default.
- W2102424853 cites W2105409495 @default.
- W2102424853 cites W2108213314 @default.
- W2102424853 cites W2109034822 @default.
- W2102424853 cites W2109899118 @default.
- W2102424853 cites W2111567059 @default.
- W2102424853 cites W2112286580 @default.
- W2102424853 cites W2112605568 @default.
- W2102424853 cites W2116437559 @default.
- W2102424853 cites W2116799923 @default.
- W2102424853 cites W2119279196 @default.
- W2102424853 cites W2122031852 @default.
- W2102424853 cites W2122621644 @default.
- W2102424853 cites W2125826054 @default.
- W2102424853 cites W2127916470 @default.
- W2102424853 cites W2130498948 @default.
- W2102424853 cites W2133006561 @default.
- W2102424853 cites W2134783591 @default.
- W2102424853 cites W2135483305 @default.
- W2102424853 cites W2137392137 @default.
- W2102424853 cites W2140479418 @default.
- W2102424853 cites W2141068458 @default.
- W2102424853 cites W2149927906 @default.