The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
Transcription Factors NRF2 and NF-κB Are Coordinated Effectors of the Rho Family, GTP-binding Protein RAC1 during Inflammation
Open accessAbstract
The small GTPase protein RAC1 participates in innate immunity by activating a complex program that includes cytoskeleton remodeling, chemotaxis, activation of NADPH oxidase, and modulation of gene expression. However, its role in regulating the transcriptional signatures that in term control the cellular inflammatory profiles are not well defined. Here we investigated the functional and mechanistic connection between RAC1 and the transcription factor NRF2 (nuclear factor erythroid 2-related factor 2), master regulator of the anti-oxidant response. Lipopolysaccharide and constitutively active RAC1(Q61L) mutant induced the anti-oxidant enzyme heme-oxygenase-1 (HO-1) through activation of NRF2. The use of KEAP1-insensitive NRF2 mutants indicated that RAC1 regulation of NRF2 is KEAP1-independent. Interestingly, NRF2 overexpression inhibited, whereas a dominant-negative mutant of NRF2 exacerbated RAC1-dependent activation of nuclear factor-κB (NF-κB), suggesting that NRF2 has an antagonistic effect on the NF-κB pathway. Moreover, we found that RAC1 acts through NF-κB to induce NRF2 because either expression of a dominant negative mutant of IκBα that leads to NF-κB degradation or the use of p65-NF-κB-deficient cells demonstrated lower NRF2 protein levels and basally impaired NRF2 signature compared with control cells. In contrast, NRF2-deficient cells showed increased p65-NF-κB protein levels, although the mRNA levels remain unchanged, indicating post-translational alterations. Our results demonstrate a new mechanism of modulation of RAC1 inflammatory pathway through a cross-talk between NF-κB and NRF2.
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Cites
NF-κB regulation in the immune system
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The Nrf2 regulatory network provides an interface between redox and intermediary metabolism
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Toll-like receptor 2–mediated NF-κB activation requires a Rac1-dependent pathway
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NF-kappa B activation by ultraviolet light not dependent on a nuclear signal
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When NRF2 Talks, Who's Listening?
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Self-citationThe Transcription Factor Nrf2 Is a Therapeutic Target against Brain Inflammation
Innamorato, N. G., Rojo, A. I., García-Yagüe, À. J., Yamamoto, M., de Ceballos, M. L., & Cuadrado, A. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.181.1.680 · Cited by 480
Self-citationStewart, D., Killeen, E., Naquin, R., Alam, S., & Alam, J. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m209195200 · Cited by 463
Cited by
Dissecting molecular cross-talk between Nrf2 and NF-κB response pathways
Wardyn, J. D., Ponsford, A. H., & Sanderson, C. M. (2015) · Biochemical Society Transactions · doi:10.1042/bst20150014 · Cited by 1,200
TNF and ROS crosstalk in inflammation
Blaser, H., Dostert, C., Mak, T. W., & Brenner, D. (2016) · Trends in Cell Biology · doi:10.1016/j.tcb.2015.12.002 · Cited by 1,008
Regulating Rho GTPases and their regulators
Hodge, R. G., & Ridley, A. J. (2016) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm.2016.67 · Cited by 872
Sivandzade, F., Prasad, S., Bhalerao, A., & Cucullo, L. (2019) · Redox Biology · doi:10.1016/j.redox.2018.11.017 · Cited by 639
Transcription Factor NRF2 as a Therapeutic Target for Chronic Diseases: A Systems Medicine Approach
Cuadrado, A., Manda, G., Hassan, A., Alcaraz, M. J., Barbas, C., Daiber, A., Ghezzi, P., León, R., López, M. G., Oliva, B., et al. (2018) · Pharmacological Reviews · doi:10.1124/pr.117.014753 · Cited by 632
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Metadata
- Authors
- Cuadrado, A., Martín-Moldes, Z., Ye, J., & Lastres-Becker, I.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2014-05
- Volume
- 289
- Issue
- 22
- Pages
- 15244-15258
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2077895679
- Cited by
- 320
- References
- 48
- FWCI
- 8.64
- Type
- journal article
- Language
- en
- Open access
- hybrid
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