A JNK-dependent pathway is required for TNFalpha-induced apoptosis.

By Yibin Deng, Xiaoyang Ren, Lin Yang, Yahong Lin, Xiangwei Wu. Cell, 2003

616 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1e6f453b376ba8d60d77ba2d32f308954ec92cd5

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. Asrar B. Malik
2. Robert F. Schwabe
3. E. Wagner
4. A. Nebreda

In Immunology

1. S. Reddy
2. Khiem A. Tran
3. D. Brenner
4. Asrar B. Malik
5. R. Kaufman
6. Robert F. Schwabe
7. R. Davis
8. M. Siddiqui

In Molecular Biology

1. R. Kaufman
2. M. Circu
3. T. Aw
4. José M. López
5. Jicheng Yue
6. A. Nebreda
7. C. Weston
8. R. Davis

Citations in the corpus

• Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, neutral): “It is not clear how JNK induces mitochondrial membrane depolarization, but it is plausible that it occurs through modifications of Bcl-2 family members [62,63], or via caspase-independent JNKmediated processing of Bid [64].”
• Interrelation of Oxidative Stress and Inflammation in Neurodegenerative Disease: Role of TNF (2015, neutral): “destabilizing the mitochondrial membrane [112, 113].”
• Mitochondrial electron transport chain, ROS generation and uncoupling (Review) (2019, neutral): “Apoptosis i) death receptor pathway: ROS-death receptors (FasL, TNF-α, TRAIL)-caspase-8-caspase-3 (87-91)”
• Integrating diverse genomic data using gene sets (2011, neutral): “The only two genes with reduced expression in the STS group are those encoding TNF, which initiates the signaling, and MAPK8, which is required for TNF-alpha-induced apoptosis [26].”
• The JNK signal transduction pathway. (2007, background): “Recent studies indicate that TNF can cause the JNK-dependent processing of Bid to a novel form (jBid) that is required for TNF-stimulated apoptosis in cells with inhibited NF-kB signaling [53].”
• Understanding MAPK Signaling Pathways in Apoptosis (2020, positive): “Intriguingly, TNFα (tumor necrosis factor alfa) treatment activates the JNK cascade, which induces caspase-8-independent cleavage of Bid; the resultant fragment of Bid (jBid), distinct to t-Bid, translocates to mitochondria and selectively promotes the release of Smac/DIABLO (second mitochondria-der”
• Mechanisms of Liver Injury. I. TNF-α-induced liver injury: role of IKK, JNK, and ROS pathways (2006, background): “Additionally, it has been suggested that JNK induces the cleavage of Bid to a specific fragment termed “jBid,” which then acts on the mitochondria to release Smac, a cofactor that is required to inhibit the TRAF2-IAP-mediated block of caspase-8 activation (8).”
• Reactive Oxygen Species in Inflammation and Tissue Injury (2014, positive): “In the absence of NF-jB, a massive accumulation of H2O2 leads to prolonged activation of JNK kinase, which induced cell death (90, 205, 369).”
• 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 (2006, background): “Released Smac binds to IAPs to promote caspase-8 activation ( 6 ).”