Autocrine Tumor Necrosis Factor Alpha Links Endoplasmic Reticulum Stress to the Membrane Death Receptor Pathway through IRE1α-Mediated NF-κB Activation and Down-Regulation of TRAF2 Expression
By P. Hu, Zhang Han, A. Couvillon, R. Kaufman, J. Exton. Molecular and Cellular Biology, 2006
772 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/ad9a4d4a0de839b59a652fbab0542d0f509f1316
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cell Biology
- R. Kaufman
- G. Hotamışlıgil
- Laurie H. Glimcher
- Ann-Hwee Lee
- C. Hetz
- Krithika Lingappan
- M. Cnop
- Decio L. Eizirik
In Molecular Biology
- G. Hotamışlıgil
- R. Kaufman
- Laurie H. Glimcher
- Ann-Hwee Lee
- Krithika Lingappan
- X. Chen
- Fabio Martinon
- A. K. Cardozo
Citations in the corpus
- Endoplasmic Reticulum Stress in Liver Disease (2010, background): “necrosis factor receptor (TNFR)-associated factor-2) (TRAF2) and apoptosis signaling kinase 1 (ASK1) to mediate the activation of c-jun N-terminal kinase (JNK) and activation of nuclear factor kappa B (NFjB) [53,135].”
- The role for endoplasmic reticulum stress in diabetes mellitus. (2008, background): “The IRE1/TRAF2 complex can also lead to NF- B activation (122, 123), which may have a pro- or antiapoptotic effect depending on the cell type and context (124).”
- NF-κB in Oxidative Stress (2017, background): “In the early phase, phosphorylation of eIF2α by PERK leads to translational suppression of I-κB [42], IRE1– TRAF2 complexes recruit IKK, leading to phosphorylation and degradation of IκB [43] and activation of the ATF6 pathway leads to phosphorylation of Akt and consequent activation of NF-κB [44].”
- Toll-like receptor activation of XBP1 regulates innate immune responses in macrophages (2010, background): “Both IRE1α and TLRs trigger the production of ROS and acute-phase proteins and both engage NEMO and TRAF adaptors to trigger inflammatory signaling components such as NF-κB and Jn”
- Aberrant Mucin Assembly in Mice Causes Endoplasmic Reticulum Stress and Spontaneous Inflammation Resembling Ulcerative Colitis (2008, background): “Activation of the ER stress response represents a plausible mechanism for induction of inflammation, since it is known to activate NF-jB [36,37], and a diminished mucus barrier is likely to increase exposure to prokaryotic-associated molecular patterns that activate immunity and antigens.”
- Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, positive): “This pathway also plays a critical role in the induction of multiple inflammatory mediators and has been implicated in insulin resistance (Deng et al., 2004; Hu et al., 2006; Shoelson et al., 2006).”