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Table representation of search results timeline featuring number of search results per year.

Year Number of Results
2006 1
2007 17
2008 41
2009 39
2010 43
2011 44
2012 61
2013 73
2014 66
2015 61
2016 62
2017 76
2018 90
2019 88
2020 72
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735 results
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Page 1
ATG16L1 orchestrates interleukin-22 signaling in the intestinal epithelium via cGAS-STING.
Aden K, Tran F, Ito G, Sheibani-Tezerji R, Lipinski S, Kuiper JW, Tschurtschenthaler M, Saveljeva S, Bhattacharyya J, Häsler R, Bartsch K, Luzius A, Jentzsch M, Falk-Paulsen M, Stengel ST, Welz L, Schwarzer R, Rabe B, Barchet W, Krautwald S, Hartmann G, Pasparakis M, Blumberg RS, Schreiber S, Kaser A, Rosenstiel P. Aden K, et al. J Exp Med. 2018 Nov 5;215(11):2868-2886. doi: 10.1084/jem.20171029. Epub 2018 Sep 25. J Exp Med. 2018. PMID: 30254094 Free PMC article.
In vivo, IL-22 treatment in Atg16l1 (ΔIEC) and Atg16l1 (ΔIEC)/Xbp1 (ΔIEC) mice potentiates endogenous ileal inflammation and causes widespread necroptotic epithelial cell death. Therapeutic blockade of IFN-I signaling ameliorates IL-22-induced ileal inflammation in …
In vivo, IL-22 treatment in Atg16l1 (ΔIEC) and Atg16l1 (ΔIEC)/Xbp1 (ΔIEC) mice potentiates endogenous ileal inflammation and c …
A Bacterial Effector Reveals the V-ATPase-ATG16L1 Axis that Initiates Xenophagy.
Xu Y, Zhou P, Cheng S, Lu Q, Nowak K, Hopp AK, Li L, Shi X, Zhou Z, Gao W, Li D, He H, Liu X, Ding J, Hottiger MO, Shao F. Xu Y, et al. Cell. 2019 Jul 25;178(3):552-566.e20. doi: 10.1016/j.cell.2019.06.007. Epub 2019 Jul 18. Cell. 2019. PMID: 31327526 Free article.
Upon bacteria-caused vacuolar damage, the V-ATPase recruited ATG16L1 onto bacteria-containing vacuole, which was blocked by SopF. ...Thus, the discovery of SopF reveals the V-ATPase-ATG16L1 axis that critically mediates autophagic recognition of intracellular pathog …
Upon bacteria-caused vacuolar damage, the V-ATPase recruited ATG16L1 onto bacteria-containing vacuole, which was blocked by SopF. ... …
Mir223 restrains autophagy and promotes CNS inflammation by targeting ATG16L1.
Li Y, Zhou D, Ren Y, Zhang Z, Guo X, Ma M, Xue Z, Lv J, Liu H, Xi Q, Jia L, Zhang L, Liu Y, Zhang Q, Yan J, Da Y, Gao F, Yue J, Yao Z, Zhang R. Li Y, et al. Autophagy. 2019 Mar;15(3):478-492. doi: 10.1080/15548627.2018.1522467. Epub 2018 Sep 22. Autophagy. 2019. PMID: 30208760 Free PMC article.
Indeed, the cellular level of Atg16l1 was decreased in BV2 cells upon Mir223 overexpression and increased following the introduction of antagomirs. We also showed that the 3' UTR of Atg16l1 contained functional Mir223-responsive sequences and that overexpression of …
Indeed, the cellular level of Atg16l1 was decreased in BV2 cells upon Mir223 overexpression and increased following the introduction …
Paneth cells as a site of origin for intestinal inflammation.
Adolph TE, Tomczak MF, Niederreiter L, Ko HJ, Böck J, Martinez-Naves E, Glickman JN, Tschurtschenthaler M, Hartwig J, Hosomi S, Flak MB, Cusick JL, Kohno K, Iwawaki T, Billmann-Born S, Raine T, Bharti R, Lucius R, Kweon MN, Marciniak SJ, Choi A, Hagen SJ, Schreiber S, Rosenstiel P, Kaser A, Blumberg RS. Adolph TE, et al. Nature. 2013 Nov 14;503(7475):272-6. doi: 10.1038/nature12599. Epub 2013 Oct 2. Nature. 2013. PMID: 24089213 Free PMC article.
Homozygosity for the highly prevalent ATG16L1 risk allele, or murine hypomorphic (HM) activity, causes Paneth cell dysfunction. As Atg16l1(HM) mice do not develop spontaneous intestinal inflammation, the mechanism(s) by which ATG16L1 contributes to disease re …
Homozygosity for the highly prevalent ATG16L1 risk allele, or murine hypomorphic (HM) activity, causes Paneth cell dysfunction. As …
New insights into the interplay between autophagy, gut microbiota and inflammatory responses in IBD.
Larabi A, Barnich N, Nguyen HTT. Larabi A, et al. Autophagy. 2020 Jan;16(1):38-51. doi: 10.1080/15548627.2019.1635384. Epub 2019 Jul 9. Autophagy. 2020. PMID: 31286804 Free PMC article.
A better understanding of the role of autophagy in IBD pathogenesis may provide better sub-classification of IBD phenotypes and novel approaches for disease management.Abbreviations: AIEC: adherent-invasive Escherichia coli; AMPK: AMP-activated protein kinase; ATF6: activating tr …
A better understanding of the role of autophagy in IBD pathogenesis may provide better sub-classification of IBD phenotypes and novel approa …
Autophagy protein ATG16L1 prevents necroptosis in the intestinal epithelium.
Matsuzawa-Ishimoto Y, Shono Y, Gomez LE, Hubbard-Lucey VM, Cammer M, Neil J, Dewan MZ, Lieberman SR, Lazrak A, Marinis JM, Beal A, Harris PA, Bertin J, Liu C, Ding Y, van den Brink MRM, Cadwell K. Matsuzawa-Ishimoto Y, et al. J Exp Med. 2017 Dec 4;214(12):3687-3705. doi: 10.1084/jem.20170558. Epub 2017 Oct 31. J Exp Med. 2017. PMID: 29089374 Free PMC article.
A variant of the autophagy gene ATG16L1 is associated with Crohn's disease, an inflammatory bowel disease (IBD), and poor survival in allogeneic hematopoietic stem cell transplant recipients. ...Intestinal organoids lacking ATG16L1 reproduced this loss in Paneth cel …
A variant of the autophagy gene ATG16L1 is associated with Crohn's disease, an inflammatory bowel disease (IBD), and poor survival in …
Mechanisms and function of autophagy in intestinal disease.
Lassen KG, Xavier RJ. Lassen KG, et al. Autophagy. 2018;14(2):216-220. doi: 10.1080/15548627.2017.1389358. Epub 2018 Jan 29. Autophagy. 2018. PMID: 29130415 Free PMC article. Review.
Distinct functions of ATG16L1 isoforms in membrane binding and LC3B lipidation in autophagy-related processes.
Lystad AH, Carlsson SR, de la Ballina LR, Kauffman KJ, Nag S, Yoshimori T, Melia TJ, Simonsen A. Lystad AH, et al. Nat Cell Biol. 2019 Mar;21(3):372-383. doi: 10.1038/s41556-019-0274-9. Epub 2019 Feb 18. Nat Cell Biol. 2019. PMID: 30778222 Free PMC article.
Here we have purified the full-length human ATG12-5-ATG16L1 complex and show its essential role in LC3B/GABARAP lipidation in vitro. ...We further show that the ATG16L1 C-terminus can compensate for WIPI2 depletion to sustain lipidation during starvation. This C-ter …
Here we have purified the full-length human ATG12-5-ATG16L1 complex and show its essential role in LC3B/GABARAP lipidation in vitro. …
An ATG16L1-dependent pathway promotes plasma membrane repair and limits Listeria monocytogenes cell-to-cell spread.
Tan JMJ, Mellouk N, Osborne SE, Ammendolia DA, Dyer DN, Li R, Brunen D, van Rijn JM, Huang J, Czuczman MA, Cemma MA, Won AM, Yip CM, Xavier RJ, MacDuff DA, Reggiori F, Debnath J, Yoshimori T, Kim PK, Fairn GD, Coyaud E, Raught B, Muise AM, Higgins DE, Brumell JH. Tan JMJ, et al. Nat Microbiol. 2018 Dec;3(12):1472-1485. doi: 10.1038/s41564-018-0293-5. Epub 2018 Nov 26. Nat Microbiol. 2018. PMID: 30478389
ATG16L1 is required for lysosome fusion with the plasma membrane and blebbing responses that promote membrane repair. ATG16L1 deficiency causes accumulation of cholesterol in lysosomes that contributes to defective membrane repair. Cell-to-cell spread by Listeria mo
ATG16L1 is required for lysosome fusion with the plasma membrane and blebbing responses that promote membrane repair. ATG16L1
Intestinal Epithelial Cell Autophagy Is Required to Protect against TNF-Induced Apoptosis during Chronic Colitis in Mice.
Pott J, Kabat AM, Maloy KJ. Pott J, et al. Cell Host Microbe. 2018 Feb 14;23(2):191-202.e4. doi: 10.1016/j.chom.2017.12.017. Epub 2018 Jan 18. Cell Host Microbe. 2018. PMID: 29358084 Free article.
Genome-wide association studies have linked polymorphisms in the autophagy gene ATG16L1 with susceptibility to inflammatory bowel disease (IBD). ...Although Atg16l1 deficiency in myeloid cells had little effect on disease, mice selectively lacking Atg16l1 in …
Genome-wide association studies have linked polymorphisms in the autophagy gene ATG16L1 with susceptibility to inflammatory bowel dis …
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