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Phosphorylation of the insulin receptor kinase by phosphocreatine in combination with hydrogen peroxide: the structural basis of redox priming

Signaling by insulin requires autophosphorylation of the insulin receptor kinase (IRK) at Tyr1158, Tyr1162, and Tyr1163. Earlier experiments with 32P‐γ‐ATP indicated that the nonphosphorylated IRK (IRK‐0P) is relatively inactive, and crystallographic data indicated that the ATP binding site of IRK‐0...

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Bibliographic Details
Main Authors: Schmid, Elmar (Author) , Hotz-Wagenblatt, Agnes (Author) , Dröge, Wulf (Author)
Format: Article (Journal)
Language:English
Published: 01 September 1999
In: The FASEB journal
Year: 1999, Volume: 13, Issue: 12, Pages: 1491-1500
ISSN:1530-6860
DOI:10.1096/fasebj.13.12.1491
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1096/fasebj.13.12.1491
Verlag, lizenzpflichtig, Volltext: https://faseb.onlinelibrary.wiley.com/doi/10.1096/fasebj.13.12.1491
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Author Notes:Elmar Schmid, Agnes Hotz‐Wagenblatt, Volker Hack, Wulf Dröge
Description
Summary:Signaling by insulin requires autophosphorylation of the insulin receptor kinase (IRK) at Tyr1158, Tyr1162, and Tyr1163. Earlier experiments with 32P‐γ‐ATP indicated that the nonphosphorylated IRK (IRK‐0P) is relatively inactive, and crystallographic data indicated that the ATP binding site of IRK‐0P is blocked by its activation loop.
Item Description:Gesehen am 09.02.2021
Physical Description:Online Resource
ISSN:1530-6860
DOI:10.1096/fasebj.13.12.1491

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