For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search

17
views
288
references
 Top references
45
cited by
 Most cited
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      194
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The Growth Hormone Receptor: Mechanism of Receptor Activation, Cell Signaling, and Physiological Aspects

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The growth hormone receptor (GHR), although most well known for regulating growth, has many other important biological functions including regulating metabolism and controlling physiological processes related to the hepatobiliary, cardiovascular, renal, gastrointestinal, and reproductive systems. In addition, growth hormone signaling is an important regulator of aging and plays a significant role in cancer development. Growth hormone activates the Janus kinase (JAK)–signal transducer and activator of transcription (STAT) signaling pathway, and recent studies have provided a new understanding of the mechanism of JAK2 activation by growth hormone binding to its receptor. JAK2 activation is required for growth hormone-mediated activation of STAT1, STAT3, and STAT5, and the negative regulation of JAK–STAT signaling comprises an important step in the control of this signaling pathway. The GHR also activates the Src family kinase signaling pathway independent of JAK2. This review covers the molecular mechanisms of GHR activation and signal transduction as well as the physiological consequences of growth hormone signaling.

          Related collections

          Most cited references 288

          • Record: found
          • Abstract: found
          • Article: not found

          Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins.

           Shona Kerr,  I Kerr,  G Stark … (1994)
          Through the study of transcriptional activation in response to interferon alpha (IFN-alpha) and interferon gamma (IFN-gamma), a previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that then phosphorylate substrate proteins called STATs (signal transducers and activators of transcription). The phosphorylated STAT proteins move to the nucleus, bind specific DNA elements, and direct transcription. Recognition of the molecules involved in the IFN-alpha and IFN-gamma pathway has led to discoveries that a number of STAT family members exist and that other polypeptide ligands also use the Jak-STAT molecules in signal transduction.
          Article 0 comments Cited 448 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Insulin-like growth factors and their binding proteins: biological actions.

             D Clemmons,  J Jones (1995)
            Article 0 comments Cited 304 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Mice carrying null mutations of the genes encoding insulin-like growth factor I (Igf-1) and type 1 IGF receptor (Igf1r).

               Jeh-Ping Liu,  Julie Baker,  Archlbald Perkins … (1993)
              Newborn mice homozygous for a targeted disruption of insulin-like growth factor gene (Igf-1) exhibit a growth deficiency similar in severity to that previously observed in viable Igf-2 null mutants (60% of normal birthweight). Depending on genetic background, some of the Igf-1(-/-) dwarfs die shortly after birth, while others survive and reach adulthood. In contrast, null mutants for the Igf1r gene die invariably at birth of respiratory failure and exhibit a more severe growth deficiency (45% normal size). In addition to generalized organ hypoplasia in Igf1r(-/-) embryos, including the muscles, and developmental delays in ossification, deviations from normalcy were observed in the central nervous system and epidermis. Igf-1(-/-)/Igf1r(-/-) double mutants did not differ in phenotype from Igf1r(-/-) single mutants, while in Igf-2(-)/Igf1r(-/-) and Igf-1(-/-)/Igf-2(-) double mutants, which are phenotypically identical, the dwarfism was further exacerbated (30% normal size). The roles of the IGFs in mouse embryonic development, as revealed from the phenotypic differences between these mutants, are discussed.
              Article 0 comments Cited 285 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Endocrinol (Lausanne)
                Journal ID (iso-abbrev): Front Endocrinol (Lausanne)
                Journal ID (publisher-id): Front. Endocrinol.
                Title: Frontiers in Endocrinology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1664-2392
                Publication date (Electronic): 13 February 2018
                Publication date Collection: 2018
                Volume: 9
                Affiliations
                1The University of Queensland Diamantina Institute, Translational Research Institute, The University of Queensland , Brisbane, QLD, Australia
                Author notes

                Edited by: Stefan N. Constantinescu, Ludwig Cancer Research, Belgium

                Reviewed by: Sandra Pellegrini, Institut Pasteur, France; Lily Huang, University of Texas Southwestern Medical Center, United States

                *Correspondence: Andrew J. Brooks, a.brooks@ 123456uq.edu.au

                Specialty section: This article was submitted to Molecular and Structural Endocrinology, a section of the journal Frontiers in Endocrinology

                Article
                DOI: 10.3389/fendo.2018.00035
                PMC ID: 5816795
                Copyright statement: Copyright © 2018 Dehkhoda, Lee, Medina and Brooks.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 6, Tables: 3, Equations: 0, References: 324, Pages: 23, Words: 20312
                Funding
                Funded by: National Health and Medical Research Council 10.13039/501100000925
                Award ID: APP1084797
                Categories
                Subject: Endocrinology
                Subject: Review

                Data availability:

                ScienceOpen disciplines: Endocrinology & Diabetes

                Keywords: growth hormone, growth hormone receptor, janus kinase 2, src family kinase, insulin-like growth factor 1, suppressor of cytokine signaling

                Comments

                Comment on this article

                Similar content 194

                See all similar

                Cited by 45

                See all cited by

                Most referenced authors 4,143

                See all reference authors