The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Regulation of glucose homeostasis through a XBP-1–FoxO1 interaction
Open accessAbstract
To date, the only known role of the spliced form of X-box–binding protein-1 (XBP-1s) in metabolic processes has been its ability to act as a transcription factor that regulates the expression of genes that increase the endoplasmic reticulum (ER) folding capacity, thereby improving insulin sensitivity. Here we show that XBP-1s interacts with the Forkhead box O1 (FoxO1) transcription factor and directs it toward proteasome-mediated degradation. Given this new insight, we tested modest hepatic overexpression of XBP-1s in vivo in mouse models of insulin deficiency or insulin resistance and found it improved serum glucose concentrations, even without improving insulin signaling or ER folding capacity. The notion that XBP-1s can act independently of its role in the ER stress response is further supported by our finding that in the severely insulin resistant ob/ob mouse strain a DNA-binding–defective mutant of XBP-1s, which does not have the ability to increase ER folding capacity, is still capable of reducing serum glucose concentrations and increasing glucose tolerance. Our results thus provide the first evidence to our knowledge that XBP-1s, through its interaction with FoxO1, can bypass hepatic insulin resistance independent of its effects on ER folding capacity, suggesting a new therapeutic approach for the treatment of type 2 diabetes.
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Cites
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
Insulin-regulated hepatic gluconeogenesis through FOXO1–PGC-1α interaction
Puigserver, P., Rhee, J., Donovan, J., Walkey, C. J., Yoon, J. C., Oriente, F., Kitamura, Y., Altomonte, J., Dong, H., Accili, D., et al. (2003) · Nature · doi:10.1038/nature01667 · Cited by 1,487
(2004) · doi:10.1016/s0092-8674(04)00452-0 · Cited by 1,356
Sriburi, R., Jackowski, S., Mori, K., & Brewer, J. W. (2004) · The Journal of Cell Biology · doi:10.1083/jcb.200406136 · Cited by 653
Nakae, J., Kitamura, T., Silver, D. L., & Accili, D. (2001) · Journal of Clinical Investigation · doi:10.1172/jci200112876 · Cited by 652
Brain IRS2 Signaling Coordinates Life Span and Nutrient Homeostasis
Taguchi, A., Wartschow, L. M., & White, M. F. (2007) · Science · doi:10.1126/science.1142179 · Cited by 523
Self-citationDong, X. C., Copps, K. D., Guo, S., Li, Y., Kollipara, R., DePinho, R. A., & White, M. F. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2008.06.006 · Cited by 463
Self-citationEndocrine regulation of ageing
Russell, S. J., & Kahn, C. R. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2234 · Cited by 356
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Almanza, A., Carlesso, A., Chintha, C., Creedican, S., Doultsinos, D., Leuzzi, B., Luís, A., McCarthy, N., Montibeller, L., More, S., et al. (2019) · The FEBS Journal · doi:10.1111/febs.14608 · Cited by 1,034
The impact of the unfolded protein response on human disease
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Metadata
- Authors
- Zhou, Y., Lee, J., Reno, C. M., Sun, C., Park, S. W., Chung, J., Lee, J., Fisher, S. J., White, M. F., Biddinger, S. B., & Ozcan, U.
- Venue
- Nature Medicine
- Published
- 2011-02-13
- Volume
- 17
- Issue
- 3
- Pages
- 356-365
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W1966157599
- Cited by
- 295
- References
- 8
- FWCI
- 11.57
- Type
- journal article
- Language
- en
- Open access
- green
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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.
