Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1.

By F. Urano, Xiaozhong Wang, A. Bertolotti, Yuhong Zhang, Peter Chung, H. Harding, D. Ron. Science, 2000

3,035 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/465371b1fce8ef3ef8c4523c4db4b50f187997cf

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. R. Kaufman
2. G. Hotamışlıgil
3. C. Hetz
4. D. Ron
5. Laurie H. Glimcher
6. J. Malhotra
7. M. Schröder
8. Peter Walter

In Molecular Biology

1. R. Kaufman
2. G. Hotamışlıgil
3. C. Hetz
4. D. Ron
5. Laurie H. Glimcher
6. M. Schröder
7. J. Malhotra
8. Ann-Hwee Lee

Citations in the corpus

• Lipid signalling in disease (2008, background): “Notably, JNK–AP-1 and IKK–NF-κB are linked to components that sense and mediate ER stress and oxidative stres”
• TRAF Family Proteins Link PKR with NF-κB Activation (2004, background): “In addition to mediating signaling in response to extracellular receptors, TRAF proteins have also been linked to JNK activation induced by endoplasmic reticulum stress via IRE1 dimerization (61).”
• A trip to the ER: coping with stress. (2004, background): “Furthermore, as well as its role in caspase-12 activation, the IRE1‐ TRAF2 interaction, which is regulated by ER stress [ 35 ], also allows for the recruitment and activation of ASK1, a stress-activated MAP3K [36], and the c-jun N-terminal kinase (JNK) [36], which might interact to initiate proapopt”
• One step at a time: endoplasmic reticulum-associated degradation (2008, background): “, a protein that is recruited to the ER membrane by the cytoplasmic tail of IRE1, one of the UPR transducers in mammalian cell”
• Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities (2008, background): “Among other functions, IRE1 and TRAF2 collaborate to activate protein kinases that have previously been implicated in immunity, inflammation and apoptosis, in particular apoptosis signal-regulating kinase 1 (ASK1; also known as MAP3K5), which causes JNK activatio”
• Autophagy Is Activated for Cell Survival after Endoplasmic ReticulumStress (2006, background): “In contrast, it is well established that JNK activation after ER stress is necessary for apoptosis induction (24, 37).”
• Reactive Oxygen Species in Health and Disease (2012, background): “the JNK signaling pathway, which is activated by various cell stressors including ROS, glucolipotoxicity, and ER stress [106–108].”
• IRE1-mediated unconventional mRNA splicing and S2P-mediated ATF6 cleavage merge to regulate XBP1 in signaling the unfolded protein response. (2002, background): “In addition, if adaptation is not sufficient, apoptosis is activated, possibly mediated by the c-Jun N-terminal protein kinase JNK, and activation of caspases 7 and 12 (Chandler et al. 1998; Nakagawa et al. 2000; Urano et al. 2000a).”
• 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].”
• IRE1α Kinase Activation Modes Control Alternate Endoribonuclease Outputs to Determine Divergent Cell Fates (2009, neutral): “IRE1α was also linked to pro-apoptotic c-Jun kinase (JNK) signaling (Urano et al., 2000).”