Activation of IKKα target genes depends on recognition of specific κB binding sites by RelB:p52 dimers

By G. Bonizzi, M. Bebien, D. Otero, Kirsten E Johnson-Vroom, Yixue Cao, D. Vu, Anil G. Jegga, Bruce J. Aronow, G. Ghosh, R. Rickert and 1 more. 2004

347 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/7c0456e1e361664f3562e3c818a0a9d4bb34a57b

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. N. Perkins
2. T. Gilmore
3. J. Campisi
4. P. Meier
5. M. Gyrd-Hansen
6. Alexander Hoffmann
7. Robert F. Schwabe
8. S. Mitchell

In Immunology

1. N. Perkins
2. T. Gilmore
3. J. Campisi
4. C. Patil
5. P. Meier
6. M. Gyrd-Hansen
7. Robert F. Schwabe
8. G. Natoli

In Oncology

1. N. Perkins
2. J. Campisi
3. P. Meier
4. M. Gyrd-Hansen
5. Robert F. Schwabe
6. G. Natoli

Citations in the corpus

• IAPs: from caspase inhibitors to modulators of NF-κB, inflammation and cancer (2010, background): “Transcription factors of the NF-κB and Rel family are activated in response to receptor stimulation and various intracellular stressors, including DNA damag”
• Signaling via the NFκB system (2016, background): “Base pair differences in κB sites may contribute to noncanonical pathway-specific gene expression.(76,77) While canonical signals transduced by NEMO require phosphorylation-dependent activation of the IKK kinase complex, noncanonical signals transduced by NIK require stabilization and accumulation o”
• Transcriptional regulation via the NF-κB signaling module (2006, background): “Intriguingly, RelB has been reported to have both positive and negative transcriptional activities (Saccani et al., 2003; Bonizzi et al., 2004; Jacque et al., 2005), but the molecular basis for alternate activities remains unknown.”
• IKKβ phosphorylates p65 at S468 in transactivaton domain 2 (2005, background): “This result is consistent with the concept that IKKα does not act through the classical pathway but mainly through RelB/p50 to target genes with a different NF-κB recognition site ( 27 ).”
• Expression of microRNA-146 suppresses NF-κB activity with reduction of metastatic potential in breast cancer cells (2008, background): “This activation of NF-κB is typically transient and limited in magnitude by numerous negative feedback loops (Akira and Takeda, 2004; Bonizzi et al., 2004; Hayden and Ghosh, 2004; Hoffmann and Baltimore, 2006).”
• Good cop, bad cop: the different faces of NF-κB (2006, background): “Different NF-kB subunit combinations have overlapping but distinct DNA-binding specificities and p52/RelB heterodimers target distinct kB elements.(16) Thus, stimuli that activate both the canonical and noncanonical pathways lead to different mixtures of subunits in the nuclear NF-kB complex, result”