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Title: Roles of linear ubiquitinylation, a crucial regulator of NF-κB and cell death, in the immune system.
Authors: Sasaki, Katsuhiro
Iwai, Kazuhiro  kyouindb  KAKEN_id  orcid (unconfirmed)
Author's alias: 岩井, 一宏
Keywords: LUBAC
linear ubiquitinylation
cell death
Issue Date: 18-Jun-2015
Publisher: wiley
Journal title: Immunological reviews
Volume: 266
Issue: 1
Start page: 175
End page: 189
Abstract: Linear ubiquitinylation, a newly identified post-translational modification, is catalyzed by the linear ubiquitin assembly complex (LUBAC), which is composed of three different subunits, HOIL-1L (heme-oxidized IRP2 ligase 1L), HOIP (HOIL-1 interacting protein), and SHARPIN (SHANK-associated RH domain-interacting protein). LUBAC plays a critical role in the activation of nuclear factor-κB (NF-κB) signaling triggered by a variety of stimuli, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and pathogen-derived components, and in the protection from cell death. Loss of function of SHARPIN in mice triggers chronic inflammation in multiple organs including the skin, as well as immunodeficiency. In humans, mutations in the gene encoding HOIL-1L cause chronic hyperinflammation and immunodeficiency, which are both associated with decreased levels of LUBAC. The linear ubiquitinylation activity of LUBAC is indispensable for B-cell function in mice, and hyperactivation of LUBAC is associated with oncogenesis in certain forms of B-cell lymphoma. In this review, the current understanding of the biochemistry of LUBAC-mediated linear ubiquitinylation and its involvement in the immune system are discussed.
Rights: This is the peer reviewed version of the following article: Sasaki, K. and Iwai, K. (2015), Roles of linear ubiquitinylation, a crucial regulator of NF-κB and cell death, in the immune system. Immunological Reviews, 266: 175–189, which has been published in final form at This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.
The full-text file will be made open to the public on 18 June 2016 in accordance with publisher's 'Terms and Conditions for Self-Archiving'.
この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。This is not the published version. Please cite only the published version.
DOI(Published Version): 10.1111/imr.12308
PubMed ID: 26085215
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