p38-dependent marking of inflammatory genes for increased NF-κB recruitment

By S. Saccani, Serafino Pantano, G. Natoli. Nature Immunology, 2002

701 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/a2c7edb7b90a9c038c36551d90b53a065a5977d7

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In Cancer Research

1. N. Perkins
2. T. Gilmore
3. Lin-Feng Chen
4. W. Greene
5. A. Mantovani
6. Y. Surh
7. A. Sica
8. J. Kundu

In Immunology

1. N. Perkins
2. A. Mantovani
3. A. Sica
4. Subhra K. Biswas
5. T. Gilmore
6. G. Natoli
7. Lin-Feng Chen
8. W. Greene

Citations in the corpus

• Regulation of the Chemokine Receptor CXCR4 by Hypoxia (2003, methodology): “ChIP assays was performed in CAOV3 cells, transiently transfected with the p(HA)HIF-1 � expression vector, and performed as described previously ( 29 ).”
• MAPK signalling pathways as molecular targets for anti-inflammatory therapy--from molecular mechanisms to therapeutic benefits. (2005, background): “p38 MAPK positively regulates expression of many genes involved in inflammation, such as those coding for TNF-a, IL-1h, IL-6, IL-8, cyclooxygenase-2, and collagenase-1, -3 [28,39,40,41,42,43,44].”
• Modulation of NF-κB Activity by Exchange of Dimers (2003, background): “Degradation of I B occurs at 10 min after stimulation, and resynthesis is complete at 2 hr (Saccani et al. 2002). n.s., nonspecific.”
• Good cop, bad cop: the different faces of NF-κB (2006, background): “p38 affects the expression of only a subset of NFkB-regulated genes and H3 Ser-10 phosphorylation appeared to target NF-kB to cryptic kB elements in promoters.(45) Thus, NF-kB modulators do not appear to be required for inducing transcription of all NF-kB target genes, but rather act selectively to ”
• Inflammation: gearing the journey to cancer. (2008, background): “inhibitory kappa B kinase (IKK)-a-mediated phosphorylation of histone-3 [59,60].”
• Integrating cell-signalling pathways with NF-κB and IKK function (2007, background): “H3 Ser10 phosphorylation is crucial for the activation of a subset of NF-κB-dependent gene”
• GADD45β/GADD45γ and MEKK4 comprise a genetic pathway mediating STAT4‐independent IFNγ production in T cells (2004, background): “Recently, p38-dependent phosphorylation of histone H3 has been shown to promote the recruitment of NF-kB, leading to the activation of certain cytokine genes (Saccani et al, 2002).”
• The IκB Kinase Complex and NF-κB Actas Master Regulators of Lipopolysaccharide-Induced Gene Expressionand Control Subordinate Activation ofAP-1 (2004, background): “For instance, in dendritic cells, p38 activity is required for LPS-induced recruitment of NF-B/p65 to a subset of target promoters (IL-6, IL-12p40, and MCP-1) ( 41 ).”
• Shaping the nuclear action of NF-κB (2004, background): “These findings raised the possibility that NF-κB activation and histone phosphorylation might be mechanistically linked in some manne”