2008
DOI: 10.1134/s0022093008050022
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Study of structural-functional arrangement of the adenylyl cyclase signaling mechanism of action of insulin-like growth factor 1 revealed in muscle tissue of representatives of vertebrates and invertebrates

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Cited by 4 publications
(3 citation statements)
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“…In fact, Willcox et al ., in a study performed on a blood‐perfused hamster cremaster muscle preparation (Willcox et al , ), reported that recombinant relaxin 2 produced a transient NO‐dependent and K + channel‐dependent vasodilation in skeletal muscle arterioles and stimulated capillaries to initiate conducted responses. This is in agreement with the suggested signalling pathway triggered by relaxin in the context of muscle tissue through receptor tyrosine kinase/Gi protein/phosphoinositide 3‐kinase/protein kinase D1/protein kinase B/NO (Plesneva et al , ).…”
Section: Effects Of Relaxin On Skeletal Musclesupporting
confidence: 91%
“…In fact, Willcox et al ., in a study performed on a blood‐perfused hamster cremaster muscle preparation (Willcox et al , ), reported that recombinant relaxin 2 produced a transient NO‐dependent and K + channel‐dependent vasodilation in skeletal muscle arterioles and stimulated capillaries to initiate conducted responses. This is in agreement with the suggested signalling pathway triggered by relaxin in the context of muscle tissue through receptor tyrosine kinase/Gi protein/phosphoinositide 3‐kinase/protein kinase D1/protein kinase B/NO (Plesneva et al , ).…”
Section: Effects Of Relaxin On Skeletal Musclesupporting
confidence: 91%
“…As previously mentioned, in the same experimental model these authors showed also a stimulating effect of insulin on AC activity, and suggested that this effect is produced through a signaling system involving both Gs and Gi proteins (Plesneva et al, 2001). Similar results were also obtained with relaxin (Shpakov et al, 2004) and insulin-like growth factor 1 (Plesneva et al, 2008), both peptides belonging to the insulin superfamily, with the only difference that in the latter case, PKC is not the PKCz isoform but another isoform close to the PKCe of the vertebrate brain.…”
Section: Membrane Receptor Agonists and The Ac/camp Systemsupporting
confidence: 78%
“…Relaxin activates the AC signaling pathway in skeletal muscles through the following signal chain: relaxin receptor tyrosine kinase → Gi protein (βγ‐dimer) → phosphatidylinositol 3‐kinase (PI3K) → protein kinase Cz (PKCζ) → heterotrimeric Gs protein → AC → protein kinase A (Kuznetsova et al., ; Shpakov et al., , , b, , ; Pertseva et al., ; Plesneva et al., ). Relaxin also activates the NO pathway in skeletal muscle via relaxin‐mediated activation of receptor tyrosine kinase → Gi protein → PI3K → protein kinase D1 → protein kinase B → NO (Plesneva et al., ). NO regulates various biological processes, and is produced by NO synthase (Stamler & Meissner, ).…”
Section: Musclementioning
confidence: 99%