Suppressor of Cytokine Signaling 1 (SOCS-1) and SOCS-3 Cause Insulin Resistance through Inhibition of Tyrosine Phosphorylation of Insulin Receptor Substrate Proteins by Discrete Mechanisms

By K. Ueki, Tatsuya Kondo, C. Kahn. Molecular and Cellular Biology, 2004

702 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/79ed3f1ff444bb9090433fd268123ae22afba283

How researchers see this paper

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

In Immunology

1. M. Febbraio
2. Jerrold M. Olefsky
3. Jaswinder K. Sethi
4. B. K. Pedersen
5. O. Osborn
6. Mitchell A. Lazar
7. W. Cawthorn
8. M. Qatanani

In Molecular Biology

1. B. K. Pedersen
2. G. Steinberg
3. Jaswinder K. Sethi
4. Jerrold M. Olefsky
5. Bruce E. Kemp
6. Mitchell A. Lazar
7. W. Cawthorn
8. M. Qatanani

In Oncology

1. Jaswinder K. Sethi
2. Jerrold M. Olefsky
3. B. K. Pedersen
4. W. Cawthorn
5. M. Febbraio

Citations in the corpus

• Interleukin-6 Increases Insulin-Stimulated Glucose Disposal in Humans and Glucose Uptake and Fatty Acid Oxidation In Vitro via AMP-Activated Protein Kinase (2006, background): “IL-6 has been shown to activate SOCS proteins in liver (41), and hepatic overexpression of SOCS1 and -3 in mice leads to liver insulin resistance (42).”
• Mechanisms of obesity-associated insulin resistance: many choices on the menu. (2007, background): “…been implicated in cytokine-mediated inhibition of insulin signaling (Emanuelli et al. 2001; Mooney et al. 2001; Rui et al. 2002), either by interfering with IRS-1 and IRS-2 tyrosine phosphorylation or by targeting IRS-1 and IRS-2 for proteosomal degradation (Rui et al. 2002; Ueki et al. 2004a).”
• TNF-α and adipocyte biology (2007, background): “Overexpression of SOCS-3 in adipose tissue causes local insulin resistance [80], whereas knockdown of SOCS-3 in adipocytes attenuates the TNF-a-mediated suppression of tyrosine phosphorylation of IRS-1 and IRS-2 [79].”
• Muscles and their myokines (2011, background): “, 2003), as SOCS-3 may directly inhibit the insulin receptor (Ueki et al., 2004).”
• Dietary factors and low-grade inflammation in relation to overweight and obesity (2011, unknown): “Another mechanism involves cytokine-induced suppressor of cytokine signalling 1 and 3, which also prevent tyrosine phosphorylation of IRS proteins, by direct interference, or ubiquitylation and subsequent degradation((130,131)).”
• The cellular and signaling networks linking the immune system and metabolism in disease (2012, background): “In cultured adipocytes, TNF-α can attenuate insulin signaling by enhancing the expression of suppressor of cytokine signaling (SOCS) proteins that bind the insulin receptor and reduce its ability to phosphorylate IRS protein”
• Energy Metabolism in the Liver (2014, unknown): “signaling is also negatively regulated by SOCS1 and SOCS3 (228, 263).”
• Disordered lipid metabolism and the pathogenesis of insulin resistance. (2007, unknown): “Suppressor of cytokine signaling 3 (SOCS3) is another potential contributor to the links among obesity, inflammation, and insulin resistance (116).”