The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Selective and antagonistic functions of SWI/SNF and Mi-2β nucleosome remodeling complexes during an inflammatory response
Open accessAbstract
Studies of mammalian genes activated in response to an acute stimulus have suggested diverse mechanisms through which chromatin structure and nucleosome remodeling events contribute to inducible gene transcription. However, because of this diversity, the logical organization of the genome with respect to nucleosome remodeling and gene induction has remained obscure. Numerous proinflammatory genes are rapidly induced in macrophages in response to microbial infection. Here, we show that in lipopolysaccharide-stimulated macrophages, the catalytic BRG1/BRM subunits of the SWI/SNF class of ATP-dependent nucleosome remodeling complexes are consistently required for the activation of secondary response genes and primary response genes induced with delayed kinetics, but not for rapidly induced primary response genes. Surprisingly, a Mi-2β complex was selectively recruited along with the SWI/SNF complexes to the control regions of secondary response and delayed primary response genes, with the Mi-2β complex acting antagonistically to limit the induction of these gene classes. SWI/SNF and Mi-2β complexes influenced cell size in a similarly antagonistic manner. These results provide insight into the differential contributions of nucleosome remodeling complexes to the rapid induction of defined classes of mammalian genes and reveal a robust anti-inflammatory function of Mi-2β.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Janeway, C. A., & Medzhitov, R. (2002) · Annual Review of Immunology · doi:10.1146/annurev.immunol.20.083001.084359 · Cited by 8,394
Toll-like receptors: critical proteins linking innate and acquired immunity
Akira, S., Takeda, K., & Kaisho, T. (2001) · Nature Immunology · doi:10.1038/90609 · Cited by 4,777
Ikaros DNA-Binding Proteins Direct Formation of Chromatin Remodeling Complexes in Lymphocytes
Kim, J., Sif, S., Jones, B., Jackson, A., Koipally, J., Heller, E., Winandy, S., Viel, A., Sawyer, A., Ikeda, T., et al. (1999) · Immunity · doi:10.1016/s1074-7613(00)80034-5 · Cited by 587
Cited by
Pattern Recognition Receptors and Inflammation
Takeuchi, O., & Akira, S. (2010) · Cell · doi:10.1016/j.cell.2010.01.022 · Cited by 8,895
Shared Principles in NF-κB Signaling
Hayden, M. S., & Ghosh, S. (2008) · Cell · doi:10.1016/j.cell.2008.01.020 · Cited by 4,494
Trained immunity: A program of innate immune memory in health and– disease
Netea, M. G., Joosten, L. A. B., Latz, E., Mills, K. H. G., Natoli, G., Stunnenberg, H. G., O’Neill, L. A. J., & Xavier, R. J. (2016) · Science · doi:10.1126/science.aaf1098 · Cited by 2,768
Transcriptional regulation of macrophage polarization: enabling diversity with identity
Lawrence, T., & Natoli, G. (2011) · Nature Reviews Immunology · doi:10.1038/nri3088 · Cited by 2,284
Diversity, Mechanisms, and Significance of Macrophage Plasticity
Locati, M., Curtale, G., & Mantovani, A. (2020) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathmechdis-012418-012718 · Cited by 2,199
Chang, P. V., Hao, L., Offermanns, S., & Medzhitov, R. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1322269111 · Cited by 2,175
NF-κB, the first quarter-century: remarkable progress and outstanding questions
Hayden, M. S., & Ghosh, S. (2012) · Genes & Development · doi:10.1101/gad.183434.111 · Cited by 1,693
Suppression of inflammation by a synthetic histone mimic
Nicodeme, E., Jeffrey, K. L., Schaefer, U., Beinke, S., Dewell, S., Chung, C.-W., Chandwani, R., Marazzi, I., Wilson, P., Coste, H., et al. (2010) · Nature · doi:10.1038/nature09589 · Cited by 1,563
Gene-specific control of inflammation by TLR-induced chromatin modifications
Foster, S. L., Hargreaves, D. C., & Medzhitov, R. (2007) · Nature · doi:10.1038/nature05836 · Cited by 1,344
Endotoxin tolerance: new mechanisms, molecules and clinical significance
Biswas, S. K., & Lopez-Collazo, E. (2009) · Trends in Immunology · doi:10.1016/j.it.2009.07.009 · Cited by 1,318
M2 Macrophage-Derived Exosomes Promote Cell Migration and Invasion in Colon Cancer
Lan, J., Sun, L., Xu, F., Liu, L., Hu, F., Song, D., Hou, Z., Wu, W., Luo, X., Wang, J., et al. (2019) · Cancer Research · doi:10.1158/0008-5472.can-18-0014 · Cited by 643
A calculated response: control of inflammation by the innate immune system
Barton, G. M. (2008) · Journal of Clinical Investigation · doi:10.1172/jci34431 · Cited by 532
Gene regulation in the immediate-early response process
Bahrami, S., & Drabløs, F. (2016) · Advances in Biological Regulation · doi:10.1016/j.jbior.2016.05.001 · Cited by 465
Polo, S. E., Kaidi, A., Baskcomb, L., Galanty, Y., & Jackson, S. P. (2010) · The EMBO Journal · doi:10.1038/emboj.2010.188 · Cited by 374
Different Neuronal Activity Patterns Induce Different Gene Expression Programs
Tyssowski, K. M., DeStefino, N. R., Cho, J.-H., Dunn, C. J., Poston, R. G., Carty, C. E., Jones, R. D., Chang, S. M., Romeo, P., Wurzelmann, M. K., et al. (2018) · Neuron · doi:10.1016/j.neuron.2018.04.001 · Cited by 390
Epigenetic regulation of the innate immune response to infection
Zhang, Q., & Cao, X. (2019) · Nature Reviews Immunology · doi:10.1038/s41577-019-0151-6 · Cited by 366
Roger, T., Lugrin, J., Le Roy, D., Goy, G., Mombelli, M., Koessler, T., Ding, X. C., Chanson, A.-L., Reymond, M. K., Miconnet, I., et al. (2011) · Blood · doi:10.1182/blood-2010-05-284711 · Cited by 341
Hu, X., Chakravarty, S. D., & Ivashkiv, L. B. (2008) · Immunological Reviews · doi:10.1111/j.1600-065x.2008.00707.x · Cited by 303
Li, X., Zhang, Q., Ding, Y., Liu, Y., Zhao, D., Zhao, K., Shen, Q., Liu, X., Zhu, X., Li, N., et al. (2016) · Nature Immunology · doi:10.1038/ni.3464 · Cited by 190
Restraint of inflammatory signaling by interdependent strata of negative regulatory pathways
Murray, P. J., & Smale, S. T. (2012) · Nature Immunology · doi:10.1038/ni.2391 · Cited by 170
Self-citationSanford, J. A., Zhang, L.-J., Williams, M. R., Gangoiti, J. A., Huang, C.-M., & Gallo, R. L. (2016) · Science Immunology · doi:10.1126/sciimmunol.aah4609 · Cited by 166
The genomic landscapes of inflammation
Natoli, G., Ghisletti, S., & Barozzi, I. (2011) · Genes & Development · doi:10.1101/gad.2018811 · Cited by 152
Role of Epigenetics in Inflammation-Associated diseases
Shanmugam, M. K., & Sethi, G. (2013) · Subcellular Biochemistry · doi:10.1007/978-94-007-4525-4_27 · Cited by 141
Predominant Interaction of Both Ikaros and Helios with the NuRD Complex in Immature Thymocytes
Sridharan, R., & Smale, S. T. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m702541200 · Cited by 130
Self-citationRole of LDB1 in the transition from chromatin looping to transcription activation
Krivega, I., Dale, R. K., & Dean, A. (2014) · Genes & Development · doi:10.1101/gad.239749.114 · Cited by 125
Class-specific Regulation of Pro-inflammatory Genes by MyD88 Pathways and IκBζ
Kayama, H., Ramirez-Carrozzi, V. R., Yamamoto, M., Mizutani, T., Kuwata, H., Iba, H., Matsumoto, M., Honda, K., Smale, S. T., & Takeda, K. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m709965200 · Cited by 92
Self-citationTerhune, S. S., Moorman, N. J., Cristea, I. M., Savaryn, J. P., Cuevas-Bennett, C., Rout, M. P., Chait, B. T., & Shenk, T. (2010) · PLoS Pathogens · doi:10.1371/journal.ppat.1000965 · Cited by 70
Glucocorticoid receptor represses proinflammatory genes at distinct steps of the transcription cycle
Gupte, R., Muse, G. W., Chinenov, Y., Adelman, K., & Rogatsky, I. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1309898110 · Cited by 70
Cutaneous innate immune tolerance is mediated by epigenetic control of MAP2K3 by HDAC8/9
Sawada, Y., Nakatsuji, T., Dokoshi, T., Kulkarni, N. N., Liggins, M. C., Sen, G., & Gallo, R. L. (2021) · Science Immunology · doi:10.1126/sciimmunol.abe1935 · Cited by 58
Epigenetic Mechanisms Governing Innate Inflammatory Responses
Perkins, D. J., Patel, M. C., Blanco, J. C. G., & Vogel, S. N. (2016) · Journal of Interferon & Cytokine Research · doi:10.1089/jir.2016.0003 · Cited by 51
Metadata
- Authors
- Ramirez-Carrozzi, V. R., Nazarian, A. A., Li, C. C., Gore, S. L., Sridharan, R., Imbalzano, A. N., & Smale, S. T.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2006-02-01
- Volume
- 20
- Issue
- 3
- Pages
- 282-296
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2142162924
- Cited by
- 422
- References
- 3
- Type
- posted content
- Language
- en
- Open access
- diamond
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
