The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Analysis of ATF3, a Transcription Factor Induced by Physiological Stresses and Modulated by gadd153/Chop10
Open accessAbstract
We demonstrate that ATF3, a member of the ATF/CREB family of transcription factors, is induced in a variety of stressed tissues: mechanically injured liver, toxin-injured liver, blood-deprived heart, and postseizure brain. We also demonstrate that an ATF3-interacting protein, gadd153/Chop10, forms a nonfunctional heterodimer with ATF3: the heterodimer, in contrast to the ATF3 homodimer, does not bind to the ATF/cyclic AMP response element consensus site and does not repress transcription. Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver's response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment. We hypothesize that in nonstressed liver, gadd153/Chop10 inhibits the limited amount of ATF3 by forming an inactive heterodimer with it, whereas in CCl4-injured liver, the synthesis of gadd153/Chop10 is repressed, allowing the induced ATF3 to function.
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Cites
Expression of c- fos Protein in Brain: Metabolic Mapping at the Cellular Level
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Independent Human MAP-Kinase Signal Transduction Pathways Defined by MEK and MKK Isoforms
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“Increasing amounts of gadd153/Chop10 were analyzed by protein-protein blotting using radiolabeled ATF3(1-100), which lacks the leucine zipper, as the probe.”
BackgroundMethodKallunki, T., Su, B., Tsigelny, I., Sluss, H. K., Dérijard, B., Moore, G., Davis, R., & Karin, M. (1994) · Genes & Development · doi:10.1101/gad.8.24.2996 · Cited by 642
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Cited by
ER-stress-induced transcriptional regulation increases protein synthesis leading to cell death
Han, J., Back, S. H., Hur, J., Lin, Y.-H., Gildersleeve, R., Shan, J., Yuan, C. L., Krokowski, D., Wang, S., Hatzoglou, M., et al. (2013) · Nature Cell Biology · doi:10.1038/ncb2738 · Cited by 1,691
Ma, Y., Brewer, J. W., Alan Diehl, J., & Hendershot, L. M. (2002) · Journal of Molecular Biology · doi:10.1016/s0022-2836(02)00234-6 · Cited by 688
Endoplasmic reticulum stress-mediated apoptosis in pancreatic β-cells
Oyadomari, S., Araki, E., & Mori, M. (2002) · Apoptosis · doi:10.1023/a:1016175429877 · Cited by 517
Tsukada, J., Yoshida, Y., Kominato, Y., & Auron, P. E. (2011) · Cytokine · doi:10.1016/j.cyto.2010.12.019 · Cited by 317
Fan, F., Jin, S., Amundson, S. A., Tong, T., Fan, W., Zhao, H., Zhu, X., Mazzacurati, L., Li, X., Petrik, K. L., et al. (2002) · Oncogene · doi:10.1038/sj.onc.1205896 · Cited by 198
Metadata
- Authors
- Chen, B. P. C., Wolfgang, C. D., & Hai, T.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 1996-03-01
- Volume
- 16
- Issue
- 3
- Pages
- 1157-1168
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2120955132
- Cited by
- 308
- References
- 4
- FWCI
- 2.52
- Type
- journal article
- Language
- en
- Open access
- green
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- Chen, B. P. C., Wolfgang, C. D., & Hai, T. (1996). Analysis of ATF3, a Transcription Factor Induced by Physiological Stresses and Modulated by gadd153/Chop10. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.16.3.1157
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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