ArticleThe Journal of biological chemistry2012
Nuclear factor-κB (NF-κB) inhibitory protein IκBβ determines apoptotic cell death following exposure to oxidative stress.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Regulation of IkappaB Protein Expression by Early Gestation in the Thymus of Ewes.Veterinary sciences · 2023Article
- β-Hydroxyisovalerylshikonin regulates macrophage polarizationPharmaceutical biology · 2022Article
- Non-cytotoxic doses of shikonin inhibit lipopolysaccharide-induced TNF-α expression via activation of the AMP-activated protein kinase signaling pathway.Experimental and therapeutic medicine · 2020Article
- Developmentally Regulated Innate Immune NFκB Signaling Mediates IL-1α Expression in the Perinatal Murine Lung.Frontiers in immunology · 2019Article
- Inhibition of IκBβ/NFκB signaling prevents LPS-induced IL1β expression without increasing apoptosis in the developing mouse lung.Pediatric research · 2017Article
- Overexpression of Hypo-Phosphorylated IκBβ at Ser313 Protects the Heart against Sepsis.PloS one · 2016Article
- Peroxisome proliferator-activated receptor γ (PPARγ) mediates the protective effect of quercetin against myocardial ischemia-reperfusion injury via suppressing the NF-κB pathway.American journal of translational research · 2016Article
- Endotoxemia Induces IκBβ/NF-κB-Dependent Endothelin-1 Expression in Hepatic Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Dynamic aberrant NF-κB spurs tumorigenesis: a new model encompassing the microenvironment.Cytokine & growth factor reviews · 2015Review
- Inhibiting IκBβ-NFκB signaling attenuates the expression of select pro-inflammatory genes.Journal of cell science · 2015Article
- Nuclear factor κB inhibition reduces lung vascular lumen obliteration in severe pulmonary hypertension in rats.American journal of respiratory cell and molecular biology · 2014Article
- Sustained hyperoxia-induced NF-κB activation improves survival and preserves lung development in neonatal mice.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- IκBβ-mediated NF-κB activation confers protection against hyperoxic lung injury.American journal of respiratory cell and molecular biology · 2014Article
- Mitochondrial retrograde signaling at the crossroads of tumor bioenergetics, genetics and epigenetics.Mitochondrion · 2013Review
- Pregnancy Weight Gain Limitation by a Supervised Nutritional Program Influences Placental NF-κB/IKK Complex Expression and Oxidative Stress.Oman medical journal · 2013Article
- The NF-κB inhibitory proteins IκBα and IκBβ mediate disparate responses to inflammation in fetal pulmonary endothelial cells.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Silencing of IkBβ mRNA causes disruption of mitochondrial retrograde signaling and suppression of tumor growth in vivo.Carcinogenesis · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The transcription factor NF-κB regulates the cellular response to inflammatory and oxidant stress. Although many studies have evaluated NF-κB activity following exposure to oxidative stress, the role of the IκB family of inhibitory proteins in modulating this activity remains unclear. Specifically, the function of IκBβ in mediating the cellular response to oxidative stress has not been evaluated. We hypothesized that blocking oxidative stress-induced NF-κB signaling through IκBβ would prevent apoptotic cell death. Using IκBβ knock-in mice (AKBI), in which the IκBα gene is replaced with the IκBβ cDNA, we show that IκBβ overexpression prevented oxidative stress-induced apoptotic cell death. This was associated with retention of NF-κB subunits in the nucleus and maintenance of NF-κB activity. Furthermore, the up-regulation of pro-apoptotic genes in WT murine embryonic fibroblasts (MEFs) exposed to serum starvation was abrogated in AKBI MEFs. Inhibition of apoptosis was observed in WT MEFs overexpressing IκBβ with simultaneous IκBα knockdown, whereas IκBβ overexpression alone did not produce this effect. These findings represent a necessary but not sufficient role of IκBβ in preventing oxidant stress-induced cell death.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.