The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
TNF‐α acts via p38 MAPK to stimulate expression of the ubiquitin ligase atrogin1/MAFbx in skeletal muscle
Open accessAbstract
Atrogin1/MAFbx is an ubiquitin ligase that mediates muscle atrophy in a variety of catabolic states. We recently found that H 2 O 2 stimulates atrogin1/MAFbx gene expression. Since the cytokine tumor necrosis factor‐α (TNF‐α) stimulates both reactive oxygen production and general activity of the ubiquitin conjugating pathway, we hypothesized that TNF‐α would also increase atrogin1/MAFbx gene expression. As with H 2 O 2 , we found that TNF‐α exposure up‐regulates atrogin1/MAFbx mRNA within2hin C2C12 myotubes. Intraperitoneal injection of TNF‐α increased atrogin1/MAFbx mRNA in skeletal muscle of adult mice within 4 h. Exposing myotubes to either TNF‐α or H 2 O 2 also produced general activation of the mitogen‐activated protein kinases (MAPKs): p38, ERK1/2, and JNK. The increase in atrogin1/MAFbx gene expression induced by TNF‐α was not altered significantly by ERK inhibitor PD98059 or the JNK inhibitor SP600125. In contrast, atrogin1/MAFbx up‐regulation and the associated increase in ubiquitin conjugating activity were both blunted by p38 inhibitors, either SB203580 or curcumin. These data suggest that TNF‐α acts via p38 to increase atrogin1/MAFbx gene expression in skeletal muscle.—Li, Y.‐P., Chen, Y., John, J., Moylan, J., Jin, B., Mann, D. L., Reid, M. B. TNF‐α acts via p38 MAPK to stimulate expression of the ubiquitin ligase atrogin1/MAFbx in skeletal muscle. FASEB J. 19, 362–370 (2005)
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Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4
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Identification of ubiquitin ligases required for skeletal muscle atrophy.
Bodine, S. C., Latres, E., Baumhueter, S., Lai, V. K.-M., Nunez, L., Clarke, B. A., Poueymirou, W. T., Panaro, F. J., Na, E., Dharmarajan, K., et al. (2001) · Science · doi:10.1126/science.1065874 · Cited by 3,521
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SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase
Bennett, B. L., Sasaki, D. T., Murray, B. W., O'Leary, E. C., Sakata, S. T., Xu, W., Leisten, J. C., Motiwala, A., Pierce, S., Satoh, Y., et al. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.251194298 · Cited by 2,558
Multiple types of skeletal muscle atrophy involve a common program of changes in gene expression
Lecker, S. H., Jagoe, R. T., Gilbert, A., Gomes, M., Baracos, V., Bailey, J., Price, S. R., Mitch, W. E., & Goldberg, A. L. (2004) · The FASEB Journal · doi:10.1096/fj.03-0610com · Cited by 1,539
What do we really know about the ubiquitin-proteasome pathway in muscle atrophy?
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Metadata
- Authors
- Li, Y.-P., Chen, Y., John, J., Moylan, J., Jin, B., Mann, D. L., & Reid, M. B.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2005-03
- Volume
- 19
- Issue
- 3
- Pages
- 362-370
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2130250591
- Cited by
- 600
- References
- 6
- FWCI
- 10.26
- Type
- journal article
- Language
- en
- Open access
- green
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- Li, Y.-P., Chen, Y., John, J., Moylan, J., Jin, B., Mann, D. L., & Reid, M. B. (2005). TNF‐α acts via p38 MAPK to stimulate expression of the ubiquitin ligase atrogin1/MAFbx in skeletal muscle. The FASEB Journal. https://doi.org/10.1096/fj.04-2364com
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