What is it about?
GH Transduction Defect is characterised by impaired GH signalling (impaired STAT3 phosphorylation) and severe short stature. Induction of the fibroblasts of patients with GHTD with higher doses of hGH is needed, compared to control fibroblasts, for successful GH signalling. We show that successful GH signalling is mediated by the activation of the EGF pathway. In addition, "catch-up" growth has been noted after hGH treatment in GHTD patients. The involvement of the EGF pathway, which is more primed in the GHTD patients than the controls, may explain the catch-up growth in the GHTD patients when exogenous GH is administered.
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Why is it important?
A new, treatable clinical entity of severe short stature is described, as well as the molecular mechanism through which treatment overcomes the defective GH signalling.
Perspectives
This publication describes the cross-talking of two fundamental signalling pathways, GH and EGF pathways, in GH Transduction Defect. Successful GH signalling is restored through the activation of an alternate pathway, that of EGF, which is highly activated in GHTD patients and results in the final phosphorylation of STAT3.
Dr Eirini Kostopoulou
University Hospital of Patras
Read the Original
This page is a summary of: Epidermal growth factor receptor (EGFR) involvement in successful growth hormone (GH) signaling in GH transduction defect, Journal of Pediatric Endocrinology and Metabolism, January 2017, De Gruyter,
DOI: 10.1515/jpem-2016-0189.
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