Matches in Nanopublications for { ?s ?p "Insulin affects cells through binding to its receptor on the surface of insulin-responsive cells. The stimulated insulin receptor phosphorylates itself and several substrates, including members of the insulin receptor substrate (IRS) family, thus initiating downstream signaling events (32, 33). The inhibition of signaling downstream of the insulin receptor is a primary mechanism through which inflammatory signaling leads to insulin resistance. Exposure of cells to TNF-a or elevated levels of free fatty acids stimulates inhibitory phosphorylation of serine residues of IRS-1" ?g. }
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- _5 value "Insulin affects cells through binding to its receptor on the surface of insulin-responsive cells. The stimulated insulin receptor phosphorylates itself and several substrates, including members of the insulin receptor substrate (IRS) family, thus initiating downstream signaling events (32, 33). The inhibition of signaling downstream of the insulin receptor is a primary mechanism through which inflammatory signaling leads to insulin resistance. Exposure of cells to TNF-a or elevated levels of free fatty acids stimulates inhibitory phosphorylation of serine residues of IRS-1" provenance.
- _5 value "Insulin affects cells through binding to its receptor on the surface of insulin-responsive cells. The stimulated insulin receptor phosphorylates itself and several substrates, including members of the insulin receptor substrate (IRS) family, thus initiating downstream signaling events (32, 33). The inhibition of signaling downstream of the insulin receptor is a primary mechanism through which inflammatory signaling leads to insulin resistance. Exposure of cells to TNF-a or elevated levels of free fatty acids stimulates inhibitory phosphorylation of serine residues of IRS-1" provenance.