Inhibition of JNK activation through NF-κB target genes

By G. Tang, Y. Minemoto, B. Dibling, N. Purcell, Zhi-wei Li, M. Karin, A. Lin. Nature, 2001

722 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/91682a9b8b85b83c3b1667125c9e19edbb13857e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. J. Moscat
2. Robert F. Schwabe
3. M. Diaz-Meco
4. A. Duran
5. Tom Luedde
6. M. Karin
7. J. Avruch
8. G. Gores

In Immunology

1. Robert F. Schwabe
2. Tom Luedde
3. M. Karin
4. J. Moscat
5. M. Diaz-Meco
6. A. Duran
7. G. Núñez
8. Y. Bae

In Molecular Biology

1. Robert F. Schwabe
2. J. Avruch
3. J. Kyriakis
4. Tom Luedde
5. J. Moscat
6. E. Shaulian
7. M. Diaz-Meco
8. A. Duran

Citations in the corpus

• To be, or not to be: NF-κB is the answer – role of Rel/NF-κB in the regulation of apoptosis (2003, background): “Several analyses found that in the absence of NF-kB, persistent JNK activity is proapoptotic (De Smaele et al., 2001; Javelaud and Besancon, 2001; Tang et al., 2001a; Lamb et al., 2003).”
• Life and death by death receptors (2009, background): “Transient JNK prodeath stimuli are normally inhibited by NF- Bregulated genes, such as xiap, which encodes the endogenous inhibitor of apoptosis, XIAP, and promotes cell survival (136).”
• AP-1 as a regulator of cell life and death (2002, background): “In addition, inhibition of JNK activity by the products of two NF-κB target-genes, Gadd45β and X-chromosome-linked inhibitor of apoptosis ( XIAP ), provides partial protection from tumour necrosis factor (TNF)-α-induced apoptosi”
• NF-κB functions as a tumour promoter in inflammation-associated cancer (2004, neutral): “JNK activation is subject to NF-κB inhibition via the NF-κB target GADD45β (ref”
• Mammalian MAPK signal transduction pathways activated by stress and inflammation: a 10-year update. (2012, background): “While this may be due in part to the elevation in JNK activation that occurs consequent to disruption of ikk (286), it is important to note, as discussed below, that neither JNK1 nor JNK2 has any hepatocyte-intrinsic effect on hepatocyte proliferation.”
• NF-κB in the liver—linking injury, fibrosis and hepatocellular carcinoma (2011, background): “The induction of cell death in the absence of NF-κB activation largely depends on a prolonged activation of JNK”
• Regulation of reactive oxygen species generation in cell signaling (2011, background): “TNF-α-induced ROS production has been also reported to play an important role in TNF-α-induced prolonged JNK activation and cell death (De Smaele et al., 2001; Ichijo et al., 1997; Matsuzawa and Ichijo, 2005; Tang et al., 2001).”