ArticleMolecular and cellular biology2005
RelA/p65 regulation of IkappaBbeta.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- ATM is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging.Aging · 2020Article
- Chemotherapy-induced muscle wasting: association with NF-κB and cancer cachexia.European journal of translational myology · 2018Article
- IκBβ enhances the generation of the low-affinity NFκB/RelA homodimer.Nature communications · 2015Article
- Prolyl-4-hydroxylase domain protein 2 controls NF-κB/p65 transactivation and enhances the catabolic effects of inflammatory cytokines on cells of the nucleus pulposus.The Journal of biological chemistry · 2015Article
- Intestinal CCL11 and eosinophilic inflammation is regulated by myeloid cell-specific RelA/p65 in mice.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Nuclear factor-κB (NF-κB) inhibitory protein IκBβ determines apoptotic cell death following exposure to oxidative stress.The Journal of biological chemistry · 2012Article
- M-CSF induces monocyte survival by activating NF-κB p65 phosphorylation at Ser276 via protein kinase C.PloS one · 2011Article
- Structure-function relationship of cytoplasmic and nuclear IκB proteins: an in silico analysis.PloS one · 2010Article
- IkappaBbeta acts to inhibit and activate gene expression during the inflammatory response.Nature · 2010Article
- IKK/NF-kappaB regulates skeletal myogenesis via a signaling switch to inhibit differentiation and promote mitochondrial biogenesis.The Journal of cell biology · 2008Article
- MAPK p38 regulates transcriptional activity of NF-kappaB in primary human astrocytes via acetylation of p65.Journal of immunology (Baltimore, Md. : 1950) · 2007Article
- NF-kappaB regulation of YY1 inhibits skeletal myogenesis through transcriptional silencing of myofibrillar genes.Molecular and cellular biology · 2007Article
- BRAP Activates Inflammatory Cascades and Increases the Risk for Carotid Atherosclerosis.Molecular medicine (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
IkappaB inhibitor proteins are the primary regulators of NF-kappaB. In contrast to the defined regulatory interplay between NF-kappaB and IkappaBalpha, much less is known regarding the regulation of IkappaBbeta by NF-kappaB. Here, we describe in detail the regulation of IkappaBbeta by RelA/p65. Using p65(-/-) fibroblasts, we show that IkappaBbeta is profoundly reduced in these cells, but not in other NF-kappaB subunit knockouts. This regulation prevails during embryonic and postnatal development in a tissue-specific manner. Significantly, in both p65(-/-) cells and tissues, IkappaBalpha is also reduced, but not nearly to the same extent as IkappaBbeta, thus highlighting the degree to which IkappaBbeta is dependent on p65. This dependence is based on the ability of p65 to stabilize IkappaBbeta protein from the 26S proteasome, a process mediated in large part through the p65 carboxyl terminus. Furthermore, IkappaBbeta was found to exist in both a basally phosphorylated and a hyperphosphorylated form. While the hyperphosphorylated form is less abundant, it is also more stable and less dependent on p65 and its carboxyl domain. Finally, we show that in p65(-/-) fibroblasts, expression of a proteolysis-resistant form of IkappaBbeta, but not IkappaBalpha, causes a severe growth defect associated with apoptosis. Based on these findings, we propose that tight control of IkappaBbeta protein by p65 is necessary for the maintenance of cellular homeostasis.
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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.