NF-κB at the crossroads of life and death

By M. Karin, A. Lin. Nature Immunology, 2002

2,642 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/30e9587415065fdd93f208e855d9e1655c8856d4

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. M. Karin
2. J. Moscat
3. M. Diaz-Meco
4. A. Duran
5. David Baltimore
6. M. Lenardo
7. Qian Zhang
8. A. Ashkenazi

In Immunology

1. M. Karin
2. Zhaoyu Jin
3. David Baltimore
4. M. Lenardo
5. Qian Zhang
6. D. Lawrence
7. Jennie Lill
8. Yun Li

Citations in the corpus

• IKKβ Is Required for Peripheral B Cell Survival and Proliferation1 (2003, background): “(48) and our present study clearly demonstrate that in addition to its established role in suppression of receptor-induced apoptosis (37), the IKK dependent canonical NF- B signaling pathway is also of importance for sustaining nonstimulated resting B cells.”
• Biphasic Dose Response in Low Level Light Therapy – an Update (2011, background): “NF-κB activation induces expression of a large number of gene products related to cell proliferation and survival (Karin and Lin 2002; Brea-Calvo et al. 2009).”
• 30 years of NF-κB: a blossoming of relevance to human pathobiology (2017, positive): “Achieving the appropriate immune response requires the NF-κB induction of apoptosis inhibitory genes (Karin and Lin, 2002).”
• Hydrogen sulfide-linked sulfhydration of NF-κB mediates its anti-apoptotic actions (2012, background): “TNF-a stimulated expression of mRNA (Figure 2C) for antiapoptotic gene targets of NF-kB, such as TRAF, cIAP2, Bcl-XL, A20, and XIAP (Karin and Lin, 2002; Wang et al., 1998), and protein levels of cIAP2 and Bcl-XL (Figure S2D) is substantially decreased in CSE knockout liver.”
• Regulation of reactive oxygen species generation in cell signaling (2011, background): “TRADD recruits TNF receptor-associated factor 2 (TRAF2), receptor-interacting protein 1 (RIP1), and cellular inhibitor of apoptosis proteins to form TNF-αinduced signaling complex I (Chen and Goeddel, 2002; Karin and Lin, 2002).”