ArticleMethods in molecular biology (Clifton, N.J.)2015
A method for the quantitative analysis of stimulation-induced nuclear translocation of the p65 subunit of NF-κB from patient-derived dermal fibroblasts.
Article in Methods in molecular biology (Clifton, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
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- Genetically programmed alternative splicing of NEMO mediates an autoinflammatory disease phenotype.The Journal of clinical investigation · 2022Article
- High-frequency near-infrared diode laser irradiation suppresses IL-1β-induced inflammatory cytokine expression and NF-κB signaling pathways in human primary chondrocytes.Lasers in medical science · 2022Article
- Development of a PHBV nanoparticle as a peptide vehicle for NOD1 activation.Drug delivery · 2021Article
- Cigarette Smoke Stimulates SARS-CoV-2 Internalization by Activating AhR and Increasing ACE2 Expression in Human Gingival Epithelial Cells.International journal of molecular sciences · 2021Article
- Chronic activation of endothelial MAPK disrupts hematopoiesis via NFKB dependent inflammatory stress reversible by SCGF.Nature communications · 2020Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Developmental and immune-mediated disease has been linked to genetic mutation of key signaling components involved in NF-κB activation that leads to impaired activation or regulation of the canonical IKK complex. We identify patients with suspected or known defects of the NF-κB signaling pathway through clinical phenotyping and genetic sequencing. To help understand how mutations cause disease, we quantitate the kinetics and dose-response of NF-κB activation signaling events in their cells. Following activation of the canonical IKK complex, phosphorylation of the inhibitor of NF-κB proteins (IκB) leads to their degradation and the subsequent translocation of NF-κB family members from the cell cytoplasm to the nucleus. Here, we provide a method to obtain patient-derived dermal fibroblasts and quantitatively assess the integrity of the signal transduction pathway from receptor activation to nuclear p65 translocation.
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Registered trials
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