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The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production

Saitoh, Tatsuya, Fujita, Naonobu, Jang, Myoung Ho, Uematsu, Satoshi, Yang, Bo-Gie, Satoh, Takashi, Omori, Hiroko, Noda, Takeshi, Yamamoto, Naoki, Komatsu, Masaaki, Tanaka, Keiji, Kawai, Taro, Tsujimura, Tohru, Takeuchi, Osamu, Yoshimori, Tamotsu, Akira, Shizuo·2008·Nature

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Crossref · 10.1038/nature07383

Cites

11 of 11 references verified0 citation errors · 0 not checkable

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Cites

Show all 11 references

Research works printed but not linked: 20

  1. Liu, Y. C., Penninger, J. & Karin, M. Immunity by ubiquitylation: A reversible process of modification. Nature Rev. Immunol. 5, 941–952 (2005) · DOI · Paper page
  2. Wang, Y. et al. Lysosome-associated small Rab GTPase Rab7b negatively regulates TLR4 signaling in macrophages by promoting lysosomal degradation of TLR4. Blood 110, 962–971 (2007) · DOI
  3. Levine, B. & Deretic, V. Unveiling the roles of autophagy in innate and adaptive immunity. Nature Rev. Immunol. 7, 767–777 (2007) · DOI · Paper page
  4. Hampe, J. et al. A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1. Nature Genet. 39, 207–211 (2007) · DOI · Paper page
  5. Akira, S., Uematsu, S. & Takeuchi, O. Pathogen recognition and innate immunity. Cell 124, 783–801 (2006) · DOI · Paper page
  6. Yamamoto, M. et al. Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway. Science 301, 640–643 (2003) · DOI · Paper page
  7. Fujita, N., Itoh, T., Fukuda, M., Noda, T. & Yoshimori, T. The Atg16L complex specifies the site of LC3 lipidation for membrane biogenesis in autophagy. Mol. Biol. Cell 19, 2092–2100 (2008) · DOI · Paper page
  8. Lee, H. K., Lund, J. M., Ramanathan, B., Mizushima, N. & Iwasaki, A. Autophagy-dependent viral recognition by plasmacytoid dendritic cells. Science 315, 1398–1401 (2007) · DOI · Paper page
  9. Kanneganti, T. D., Lamkanfi, M. & Núñez, G. Intracellular NOD-like receptors in host defense and disease. Immunity 27, 549–559 (2007) · DOI · Paper page
  10. Hsu, L. C. et al. The protein kinase PKR is required for macrophage apoptosis after activation of Toll-like receptor 4. Nature 428, 341–345 (2004) · DOI · Paper page
  11. Greten, F. R. et al. NF-κB is a negative regulator of IL-1β secretion as revealed by genetic and pharmacological inhibition of IKKβ. Cell 130, 918–931 (2007) · DOI · Paper page
  12. Hewinson, J., Moore, S. F., Glover, C., Watts, A. G. & MacKenzie, A. B. A key role for redox signaling in rapid P2X7 receptor-induced IL-1beta processing in human monocytes. J. Immunol. 180, 8410–8420 (2008) · DOI
  13. Xu, Y. et al. Toll-like receptor 4 is a sensor for autophagy associated with innate immunity. Immunity 27, 135–144 (2007) · DOI · Paper page
  14. Delgado, M. A., Elmaoued, R. A., Davis, A. S., Kyei, G. & Deretic, V. Toll-like receptors control autophagy. EMBO J. 27, 1110–1121 (2008) · DOI · Paper page
  15. Komatsu, M. et al. Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice. Cell 131, 1149–1163 (2007) · DOI · Paper page
  16. Maeda, S. et al. Nod2 mutation in Crohn's disease potentiates NF-κB activity and IL-1β processing. Science 307, 737–738 (2005)
  17. Ishikura, T. et al. Interleukin-18 overproduction exacerbates the development of colitis with markedly infiltrated macrophages in interleukin-18 transgenic mice. J. Gastroenterol. Hepatol. 18, 960–969 (2003) · DOI
  18. Izcue, A., Coombes, J. L. & Powrie, F. Regulatory T cells suppress systemic and mucosal immune activation to control intestinal inflammation. Immunol. Rev. 212, 256–271 (2006) · DOI · Paper page
  19. Nakagawa, I. et al. Autophagy defends cells against invading group A Streptococcus. Science 306, 1037–1040 (2004) · DOI · Paper page
  20. Fujita, N. et al. An Atg4B mutant hampers the lipidation of LC3 paralogues and causes defects in autophagosome closure. Mol. Biol. Cell advance online publication, doi: 10.1091/mbc.E08-03-0312 (3 September 2008) · DOI · Paper page

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Metadata

Authors
Saitoh, T., Fujita, N., Jang, M. H., Uematsu, S., Yang, B.-G., Satoh, T., Omori, H., Noda, T., Yamamoto, N., Komatsu, M., Tanaka, K., Kawai, T., Tsujimura, T., Takeuchi, O., Yoshimori, T., & Akira, S.
Venue
Nature
Published
2008-10-05
Volume
456
Issue
7219
Pages
264-268
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
OpenAlex
W2064741210
Cited by
2,014
References
11
FWCI
60.44
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)

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CoChat. (2026). Citation check: Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production. https://app.cochat.ai/papers/10.1038/nature07383
The paper
Saitoh, T., Fujita, N., Jang, M. H., Uematsu, S., Yang, B.-G., Satoh, T., Omori, H., Noda, T., Yamamoto, N., Komatsu, M., Tanaka, K., Kawai, T., Tsujimura, T., Takeuchi, O., Yoshimori, T., & Akira, S. (2008). Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production. Nature. https://doi.org/10.1038/nature07383

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.