The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
UPR Pathways Combine to Prevent Hepatic Steatosis Caused by ER Stress-Mediated Suppression of Transcriptional Master Regulators
Open accessAbstract
Summary The unfolded protein response (UPR) is linked to metabolic dysfunction, yet it is not known how ER disruption might influence metabolic pathways. Using a multilayered genetic approach, we find that mice with genetic ablations of either ER stress sensing pathways (ATF6α, eIF2α, IRE1α), or of ER quality control (p58IPK), share a common dysregulated response to ER stress that includes the development of microvesicular steatosis. The rescue of ER protein processing capacity by the combined action of UPR pathways during stress prevents the suppression of a subset of metabolic transcription factors that regulate lipid homeostasis. This suppression occurs in part by unresolved ER stress perpetuating expression of the transcriptional repressor CHOP. As a consequence, metabolic gene expression networks are directly responsive to ER homeostasis. These results reveal an unanticipated direct link between ER homeostasis and the transcriptional regulation of metabolism and suggest mechanisms by which ER stress might underlie microvesicular steatosis.
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1 retracted
Proapoptotic BAX and BAK Modulate the Unfolded Protein Response by a Direct Interaction with IRE1α
Hetz, C., Bernasconi, P., Fisher, J., Lee, A.-H., Bassik, M. C., Antonsson, B., Brandt, G. S., Iwakoshi, N. N., Schinzel, A., Glimcher, L. H., et al. (2006) · Science · doi:10.1126/science.1123480 · Cited by 667
RetractedSignal integration in the endoplasmic reticulum unfolded protein response
Ron, D., & Walter, P. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2199 · Cited by 6,296
Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes
Özcan, U., Cao, Q., Yilmaz, E., Lee, A.-H., Iwakoshi, N. N., Özdelen, E., Tuncman, G., Görgün, C., Glimcher, L. H., & Hotamisligil, G. S. (2004) · Science · doi:10.1126/science.1103160 · Cited by 3,844
An Integrated Stress Response Regulates Amino Acid Metabolism and Resistance to Oxidative Stress
Harding, H. P., Zhang, Y., Zeng, H., Novoa, I., Lu, P. D., Calfon, M., Sadri, N., Yun, C., Popko, B., Paules, R., et al. (2003) · Molecular Cell · doi:10.1016/s1097-2765(03)00105-9 · Cited by 3,323
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Metabolic control through the PGC-1 family of transcription coactivators
Lin, J., Handschin, C., & Spiegelman, B. M. (2005) · Cell Metabolism · doi:10.1016/j.cmet.2005.05.004 · Cited by 2,130 · cited 1×
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BackgroundZinszner, H., Kuroda, M., Wang, X., Batchvarova, N., Lightfoot, R. T., Remotti, H., Stevens, J. L., & Ron, D. (1998) · Genes & Development · doi:10.1101/gad.12.7.982 · Cited by 2,014
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Translational Control Is Required for the Unfolded Protein Response and In Vivo Glucose Homeostasis
Scheuner, D., Song, B., McEwen, E., Liu, C., Laybutt, R., Gillespie, P., Saunders, T., Bonner-Weir, S., & Kaufman, R. J. (2001) · Molecular Cell · doi:10.1016/s1097-2765(01)00265-9 · Cited by 1,355
Self-citation
Cited by
Endoplasmic reticulum stress and the inflammatory basis of metabolic disease
Hotamisligil, G. S. (2010) · Cell · doi:10.1016/j.cell.2010.02.034 · Cited by 2,802
Mechanisms, regulation and functions of the unfolded protein response
Hetz, C., Zhang, K., & Kaufman, R. J. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-0250-z · Cited by 2,666
Self-citationDynamics and functions of lipid droplets
Olzmann, J. A., & Carvalho, P. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-018-0085-z · Cited by 2,740
Inflammation in obesity, diabetes, and related disorders
Rohm, T. V., Meier, D. T., Olefsky, J. M., & Donath, M. Y. (2022) · Immunity · doi:10.1016/j.immuni.2021.12.013 · Cited by 2,066
Kaser, A., Zeissig, S., & Blumberg, R. S. (2010) · Annual Review of Immunology · doi:10.1146/annurev-immunol-030409-101225 · Cited by 1,806
Metadata
- Authors
- Rutkowski, D. T., Wu, J., Back, S.-H., Callaghan, M. U., Ferris, S. P., Iqbal, J., Clark, R., Miao, H., Hassler, J. R., Fornek, J., Katze, M. G., Hussain, M. M., Song, B., Swathirajan, J., Wang, J., Yau, G. D.-Y., & Kaufman, R. J.
- Venue
- Developmental Cell
- Publisher
- Elsevier BV
- Published
- 2008-12
- Volume
- 15
- Issue
- 6
- Pages
- 829-840
- ISSN
- 1534-5807 (ISSN-L)
- OpenAlex
- W2095968062
- Cited by
- 580
- References
- 47
- FWCI
- 13.01
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Rutkowski, D. T., Wu, J., Back, S.-H., Callaghan, M. U., Ferris, S. P., Iqbal, J., Clark, R., Miao, H., Hassler, J. R., Fornek, J., Katze, M. G., Hussain, M. M., Song, B., Swathirajan, J., Wang, J., Yau, G. D.-Y., & Kaufman, R. J. (2008). UPR Pathways Combine to Prevent Hepatic Steatosis Caused by ER Stress-Mediated Suppression of Transcriptional Master Regulators. Developmental Cell. https://doi.org/10.1016/j.devcel.2008.10.015
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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.