NF-kappaB-induced loss of MyoD messenger RNA: possible role in muscle decay and cachexia.

By D. Guttridge, Marty W. Mayo, L. Madrid, Cun-Yu Wang, A. Baldwin. Science, 2000

986 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/dbdaeb5f1d87efc0a1e7e05800ab812e97c07d49

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Richard J. Johnson
2. G. Semenza

In Molecular Biology

1. K. Fearon
2. D. Glass
3. Richard J. Johnson
4. D. Guttridge
5. G. Semenza
6. J. Hawley
7. Vernon G. Coffey

Citations in the corpus

• The molecular basis of skeletal muscle atrophy. (2004, background): “Another group has shown that TNF- plus IFN- -induced NF- B activation leads to downregulation of MyoD protein at a posttranslational level, which in turn may lead to decreased myofibrillar synthesis (33).”
• Systemic effects of chronic obstructive pulmonary disease (2003, background): “MyoD and MEF-2, as well as CBP/p300 and HDAC5, have very recently been shown to play a fundamental role in the failure of muscle cells to regenerate after injury in patients with cancer cachexia [119, 120].”
• IκBα and p65 Regulate the Cytoplasmic Shuttling of Nuclear Corepressors: Cross-talk between Notch and NFκB Pathways (2003, background): “Both Notch and NF B pathways are involved in the regulation of gene expression and differentiation in many different systems (Egan et al., 1998; Feng and Porter, 1999; Kaliman et al., 1999; Guttridge et al., 2000; Kaisho et al., 2001), including hematopoietic cells (Boothby et al.”
• Cancer cachexia: mediators, signaling, and metabolic pathways. (2012, background): “In vitro, TNFa inhibits both adipocyte and skeletal myocyte differentiation (Guttridge et al., 2000; Ruan et al., 2002) and contributes to insulin resistance in part by impinging on the insulin signaling pathway (Hotamisligil, 1999).”
• IL-10, IL-6, and TNF-alpha: central factors in the altered cytokine network of uremia--the good, the bad, and the ugly. (2005, background): “TNF-α has been shown to activate the transcription factor NF-κB to suppress MyoD mRNA at the posttranscriptional level, thus disrupting skeletal muscle differentiation and repair of damaged muscle tissu”
• Skeletal muscle hypertrophy and atrophy signaling pathways. (2005, background): “The TNF -inhibition of myogenesis was postulated to inhibit the ability of muscle precursor, or “satellite,” cells to be recruited into the muscle, further enhancing the atrophic effect (Guttridge et al., 2000).”
• IKKβ phosphorylates p65 at S468 in transactivaton domain 2 (2005, neutral): “Marty Mayo, University of Virginia) have been described previously (16, 22).”