ArticleMolecular and cellular biology2003
Regulation of c-Rel nuclear localization by binding of Ca2+/calmodulin.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 52 citations in OpenAlex.
- Sensing danger through a "finger".The Journal of experimental medicine · 2018Article
- STIM- and Orai-mediated calcium entry controls NF-κB activity and function in lymphocytes.Cell calcium · 2018Review
- Nesprin-2 mediated nuclear trafficking and its clinical implications.Nucleus (Austin, Tex.) · 2015Article
- The role of calcium, NF-κB and NFAT in the regulation of CXCL8 and IL-6 expression in Jurkat T-cells.International journal of biochemistry and molecular biology · 2013Article
- Lipopolysaccharide induces endoplasmic store Ca2+-dependent inflammatory responses in lung microvessels.PloS one · 2013Article
- Involvement of calmodulin and calmodulin kinase II in tumor necrosis factor alpha-induced survival of bone marrow derived macrophages.Biochemical and biophysical research communications · 2012Article
- Specific nuclear localizing sequence directs two myosin isoforms to the cell nucleus in calmodulin-sensitive manner.PloS one · 2012Article
- The c-Rel Transcription Factor in Development and Disease.Genes & cancer · 2011Article
- A cytosolic STIM2 preprotein created by signal peptide inefficiency activates ORAI1 in a store-independent manner.The Journal of biological chemistry · 2011Article
- Differential cytokine regulation by NF-kappaB and AP-1 in Jurkat T-cells.BMC immunology · 2010Article
- Calmodulin-driven nuclear entry: trigger for sex determination and terminal differentiation.The Journal of biological chemistry · 2009Review
- Activation of AMP-activated protein kinase by human EGF receptor 2/EGF receptor tyrosine kinase inhibitor protects cardiac cells.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Induced TRPC1 expression sensitizes intestinal epithelial cells to apoptosis by inhibiting NF-kappaB activation through Ca2+ influx.The Biochemical journal · 2006Article
- Functional link between TNF biosynthesis and CaM-dependent activation of inducible nitric oxide synthase in RAW 264.7 macrophages.American journal of physiology. Cell physiology · 2006Article
- Calcium-dependent regulation of the cell cycle via a novel MAPK--NF-kappaB pathway in Swiss 3T3 cells.The Journal of cell biology · 2004Article
- The clinical implication and molecular mechanism of preferential IL-4 production by modified glycolipid-stimulated NKT cells.The Journal of clinical investigation · 2004Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NF-kappa B/Rel family of transcription factors participates in the control of a wide array of genes, including genes involved in embryonic development and regulation of immune, inflammation, and stress responses. In most cells, inhibitory I kappa B proteins sequester NF-kappa B/Rel in the cytoplasm. Cellular stimulation results in the degradation of I kappa B and modification of NF-kappa B/Rel proteins, allowing NF-kappa B/Rel to translocate to the nucleus and act on its target genes. Calmodulin (CaM) is a highly conserved, ubiquitously expressed Ca(2+) binding protein that serves as a key mediator of intracellular Ca(2+) signals. Here we report that two members of the NF-kappa B/Rel family, c-Rel and RelA, interact directly with Ca(2+)-loaded CaM. The interaction with CaM is greatly enhanced by cell stimulation, and this enhancement is blocked by addition of I kappa B. c-Rel and RelA interact with CaM through a similar sequence near the nuclear localization signal. Compared to the wild-type protein, CaM binding-deficient mutants of c-Rel exhibit increases in both nuclear accumulation and transcriptional activity on the interleukin 2 and granulocyte macrophage colony-stimulating factor promoters in the presence of a Ca(2+) signal. Conversely, for RelA neither nuclear accumulation nor transcriptional activity on these promoters is increased by mutation of the sequence interacting with CaM. Our results suggest that CaM binds c-Rel and RelA after their release from I kappa B and can inhibit nuclear import of c-Rel while letting RelA translocate to the nucleus and act on its target genes. CaM can therefore differentially regulate the activation of NF-kappa B/Rel proteins following stimulation.
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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.