Translational Repression Mediates Activation of Nuclear Factor Kappa B by Phosphorylated Translation Initiation Factor 2

By Jing Deng, Phoebe D. Lu, Yuhong Zhang, D. Scheuner, R. Kaufman, Nahum Sonenberg, H. Harding, D. Ron. Molecular and Cellular Biology, 2004

663 citations recorded by the source corpus.

Subfields: Cell Biology, Infectious Diseases, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d113644e3f4cad356a7d789b46ed408a86cc377e

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

1. É. Chevet
2. C. Hetz
3. G. Burton
4. A. K. Cardozo
5. Krithika Lingappan
6. M. Cnop
7. Eric Jauniaux
8. Decio L. Eizirik

In Molecular Biology

1. G. Burton
2. É. Chevet
3. A. K. Cardozo
4. C. Hetz
5. Krithika Lingappan
6. M. Cnop
7. Eric Jauniaux
8. Decio L. Eizirik

Citations in the corpus

• Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, neutral): “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).”
• The integrated stress response (2016, neutral): “Translational repression by eIF2 a has also been implicated in nuclear factor kappa light chain enhancer of activated B cells (NF-j B) pathway induction to protect against ER stress [186].”
• The eIF2α kinases: their structures and functions (2013, neutral): “The mechanism by which eIF2α activates NF-κB appears to be largely due to decreased synthesis of the inhibitory proteins of NF-κB, the IκBs [42].”
• 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.”
• Autophagy and the integrated stress response (2010, neutral): “PERK may also reduce the translation of IkBa (Deng et al., 2004), thereby activating NF-kB, which also could contribute to autophagy (Figure 4B).”
• Pathophysiology of placental‐derived fetal growth restriction (2018, background): “The half-life of the inhibitor of kappa B (IkB) subunit is shorter than that of NFkB, and so prolonged translational arrest will inevitably lead to an inflammatory response.(93) Proinflammatory”
• Endoplasmic reticulum stress signalling and the pathogenesis of non-alcoholic fatty liver disease. (2018, background): “15 PERK branch reduces translation of IkB, increasing NF-kB activity (104, 105).”
• 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].”