The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
ERK1/2 and p38-MAPK signalling pathways, through MSK1, are involved in NF-κB transactivation during oxidative stress in skeletal myoblasts
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Citations
Cites
Hayden, M. S., & Ghosh, S. (2004) · Genes & Development · doi:10.1101/gad.1228704 · Cited by 3,842
Missing Pieces in the NF-κB Puzzle
Ghosh, S., & Karin, M. (2002) · Cell · doi:10.1016/s0092-8674(02)00703-1 · Cited by 3,638
Mammalian thioredoxin is a direct inhibitor of apoptosis signal‐regulating kinase (ASK) 1
Saitoh, M., Nishitoh, H., Fujii, M., Takeda, K., Tobiume, K., Sawada, Y., Kawabata, M., Miyazono, K., & Ichijo, H. (1998) · The EMBO Journal · doi:10.1093/emboj/17.9.2596 · Cited by 2,377
Free radicals and tissue damage produced by exercise
Davies, K. J. A., Quintanilha, A. T., Brooks, G. A., & Packer, L. (1982) · Biochemical and Biophysical Research Communications · doi:10.1016/s0006-291x(82)80124-1 · Cited by 1,739
Takada, Y., Mukhopadhyay, A., Kundu, G. C., Mahabeleshwar, G. H., Singh, S., & Aggarwal, B. B. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m212389200 · Cited by 495
Mechanisms of disuse muscle atrophy: role of oxidative stress
Powers, S. K., Kavazis, A. N., & DeRuisseau, K. C. (2005) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00469.2004 · Cited by 368
Baeza-Raja, B., & Muñoz-Cánoves, P. (2004) · Molecular Biology of the Cell · doi:10.1091/mbc.e03-08-0585 · Cited by 247
Cited by
The mechanisms of muscle hypertrophy and their application to resistance training
Schoenfeld, B. J. (2010) · Journal of Strength and Conditioning Research · doi:10.1519/jsc.0b013e3181e840f3 · Cited by 1,214
Opportunities and challenges of radiotherapy for treating cancer
Schaue, D., & McBride, W. H. (2015) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2015.120 · Cited by 784
Salminen, A., Kauppinen, A., & Kaarniranta, K. (2012) · Cellular Signalling · doi:10.1016/j.cellsig.2011.12.006 · Cited by 763
The Role of Inflammation in Age-Related Sarcopenia
Dalle, S., Rossmeislova, L., & Koppo, K. (2017) · Frontiers in Physiology · doi:10.3389/fphys.2017.01045 · Cited by 668
Redox Mechanism of Reactive Oxygen Species in Exercise
He, F., Li, J., Liu, Z., Chuang, C.-C., Yang, W., & Zuo, L. (2016) · Frontiers in Physiology · doi:10.3389/fphys.2016.00486 · Cited by 385
Metadata
- Authors
- Kefaloyianni, E., Gaitanaki, C., & Beis, I.
- Venue
- Cellular Signalling
- Publisher
- Elsevier BV
- Published
- 2006-12
- Volume
- 18
- Issue
- 12
- Pages
- 2238-2251
- ISSN
- 0898-6568 (ISSN-L)
- OpenAlex
- W1987217810
- Cited by
- 257
- References
- 7
- FWCI
- 7.32
- Type
- journal article
- Language
- en
- Open access
- closed
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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.
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- CoChat. (2026). Citation check: ERK1/2 and p38-MAPK signalling pathways, through MSK1, are involved in NF-κB transactivation during oxidative stress in skeletal myoblasts. https://app.cochat.ai/papers/10.1016/j.cellsig.2006.05.004
- The paper
- Kefaloyianni, E., Gaitanaki, C., & Beis, I. (2006). ERK1/2 and p38-MAPK signalling pathways, through MSK1, are involved in NF-κB transactivation during oxidative stress in skeletal myoblasts. Cellular Signalling. https://doi.org/10.1016/j.cellsig.2006.05.004
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.
