IKKbeta/NF-kappaB activation causes severe muscle wasting in mice.

By D. Cai, J. Frantz, N. Tawa, P. A. Meléndez, Byung-Chul Oh, H. Lidov, P. Hasselgren, W. Frontera, Jongsoon Lee, D. Glass and 1 more. Cell, 2004

819 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4415e8721279d939d1b777189ce95608386f2c09

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In Molecular Biology

1. M. Sandri
2. S. Schiaffino
3. A. Goldberg
4. P. Bonaldo
5. C. Mammucari
6. D. Glass
7. B. K. Pedersen
8. S. Lecker

Citations in the corpus

• NF-κB activation as a pathological mechanism of septic shock and inflammation (2006, neutral): “As discussed above, NF- B activation contributes to the development of muscle wasting, which is another feature of septic shock (29).”
• The E3 Ligase MuRF1 degrades myosin heavy chain protein in dexamethasone-treated skeletal muscle. (2007, background): “…or the upregulation of constitutively active IKK, in which MuRF1 deletion has been previously shown to block atrophy (Bodine et al., 2001; Cai et al., 2004), DEX treatment of MuRF1 null animals did not result in a statistically significant decrease in atrophy in comparison to DEX…”
• Protein degradation by the ubiquitin-proteasome pathway in normal and disease states. (2006, background): “When activated, FoxO and NF- B cause profound muscle wasting through induction of these E3s together with other atrogenes (75,82,83).”
• Molecular Inflammation: Underpinnings of Aging and Age-related Diseases (2008, background): “Furthermore, inhibitors of NF-κB have been shown to attenuate body weight loss and protein degradation in skeletal muscle (Cai et al., 2004).”
• An official American Thoracic Society/European Respiratory Society statement: update on limb muscle dysfunction in chronic obstructive pulmonary disease. (2014, background): “Through transcriptional activities of nuclear factor-kappa B (NF-kB) and forkhead box O (FOXO) (136),”
• Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy (2020, background): “Transgenic overexpression of activated IκB kinase β (IKKβ) in skeletal muscle caused profound muscle wasting, with increased expression of MuRF1 but not MAFbx/Atrogin-1 [35].”
• Cellular and molecular mechanisms of muscle atrophy (2013, background): “…al., 2010 KO No phenotype, but protection from denervation-induced atrophy Mittal et al., 2010 IKK (IKK2) Muscle-specific transgenic Muscle atrophy Cai et al., 2004 Muscle-specific KO Increased muscle strength, protection from denervationinduced atrophy Mourkioti et al., 2006 p105/p50 (Nfkb1) KO…”
• Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models (2011, background): “Circulating cytokines, such as TNFa and TNF-related weak inducer of apoptosis (TWEAK), can activate MuRF1 via the transcription factor nuclear factor B (NF B) [32,33].”
• Muscle as an endocrine organ: focus on muscle-derived interleukin-6. (2008, result): “In favor of the before-mentioned studies, demonstrating that the NF B signaling pathway is not activated by contraction in human skeletal muscle (60, 337), it was shown that the I B kinase beta (I K ) does not increase the transcription of IL-6 (46), suggesting that IL-6 gene transcription in skelet”
• Integrating Mechanisms for Insulin Resistance: Common Threads and Missing Links (2012, neutral): “Inappropriate activation of the IKK/NF-k B pathway, as seen in mice with muscle-specific over-expression of IKK-b (MIKK mice), can lead to muscle atrophy (Cai et al., 2004).”
• FoxO3 controls autophagy in skeletal muscle in vivo. (2007, background): “The discrepancy between the results presented here and previous studies with respect to the role of mTOR in autophagy might also reflect the slower pace of autophagy in vivo, based on Fasting-induced autophagy is not impaired in adult skeletal muscle of atrogin-1 null (A) or MuRF1 null (B) mice.”