NF-kappaB at the crossroads of life and death.

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

1,156 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c90ab64cd3954e9d66e2c48d72909c197de800ed

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Citations in the corpus

Reactive oxygen species in tumor progression. (2005, background): “1888 regulation of NF-κB has been extensively studied during the last decade mostly by analyzing cytokine-mediated activation mechanisms (165-167).”
CD28 costimulation improves expansion and persistence of chimeric antigen receptor-modified T cells in lymphoma patients. (2011, background): “One strategy to achieve this goal takes advantage of members of the tumor necrosis family (TNF) to recruit specific TNF-receptor-associated factor (TRAF) adapter proteins, which represents a fundamental departure from CD28 costimulation (23).”
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).”
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).”
NF-κB represses E-cadherin expression and enhances epithelial to mesenchymal transition of mammary epithelial cells: potential involvement of ZEB-1 and ZEB-2 (2007, background): “To determine whether NF-kB when activated under more physiological conditions could induce the EMT phenotype, MCF10A cells were continuously cultured in medium containing TNFa, a known activator of NF-kB (Karin and Lin, 2002).”
30 years of NF-κB: a blossoming of relevance to human pathobiology (2017, unknown): “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.”
Common SNP in pre-miR-146a decreases mature miR expression and predisposes to papillary thyroid carcinoma (2008, background): “The NF-kappa B pathway is critical for tumor formation because it promotes not only cell survival by the expression of antiapoptotic proteins, but also the transcription of many immunerelated genes and proinflammatory cytokines that can influence tumor progression through the mobilization of host ce”
Heterologous immunity provides a potent barrier to transplantation tolerance. (2003, background): “Interestingly, NF-κB plays a critical role in determining the balance between pro- and antiapoptotic factors, which in turn determine the fate of the cell (42, 43).”
Apo2L/TRAIL and its death and decoy receptors (2003, background): “overcome in many cell types for TNF to induce apoptosis (reviewed in Wu et al.(62)).”
Redox Regulation of Cell Survival (2008, unknown): “TNF receptor–associated factor TRAF1; (e) Gadd45, which inhibits JNK-mediated cell death; and (f) antioxidants such as Mn-SOD and ferritin heavy chain (FHC) (147).”