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Epidermal growth factor receptor juxtamembrane region regulates allosteric tyrosine kinase activation
Journal article   Open access   Peer reviewed

Epidermal growth factor receptor juxtamembrane region regulates allosteric tyrosine kinase activation

Kristina W. Thiel and Graham Carpenter
Proceedings of the National Academy of Sciences - PNAS, Vol.104(49), pp.19238-19243
12/04/2007
DOI: 10.1073/pnas.0703854104
PMCID: PMC2148274
PMID: 18042729
url
https://doi.org/10.1073/pnas.0703854104View
Published (Version of record) Open Access

Abstract

Structural studies of the extracellular and tyrosine kinase domains of the epidermal growth factor receptor (ErbB-1) provide considerable insight into facets of the receptor activation mechanism, but the contributions of other regions of ErbB-1 have not been ascertained. This study demonstrates that the intracellular juxtamembrane (JM) region plays a vital role in the kinase activation mechanism. In the experiments described herein, the entire ErbB-1 intracellular domain (ICD) has been expressed in mammalian cells to explore the significance of the JM region in kinase activity. Deletion of the JM region (ΔJM) results in a severe loss of ICD tyrosine phosphorylation, indicating that this region is required for maximal activity of the tyrosine kinase domain. Coexpression of ΔJM and dimerization-deficient kinase domain ICD mutants revealed that the JM region is indispensable for allosteric kinase activation and productive monomer interactions within a dimer. Studies with the intact receptor confirmed the role of the JM region in kinase activation. Within the JM region, Thr-654 is a known protein kinase C (PKC) phosphorylation site that modulates kinase activity in the context of the intact ErbB-1 receptor; yet, the mechanism is not known. Whereas a T654A mutation promotes increased ICD tyrosine phosphorylation, the phosphomimetic T654D mutant generates a 50% reduction in ICD tyrosine phosphorylation. Similar to the ΔJM mutants, the T654D mutant ICD failed to interact with a wild-type monomer. This study reveals an integral role for the intracellular JM region of ErbB-1 in allosteric kinase activation.
Biological Sciences

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