Insulin-Like Growth Factor 1 Receptor Signaling Regulates Skin Development and Inhibits Skin Keratinocyte Differentiation

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Published inMolecular and Cellular Biology Vol. 26; no. 7; pp. 2675 - 2687
Main Authors Sadagurski, Marianna, Yakar, Shoshana, Weingarten, Galina, Holzenberger, Martin, Rhodes, Christopher J., Breitkreutz, Dirk, LeRoith, Derek, Wertheimer, Efrat
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.04.2006
Taylor & Francis
Subjects
Animals
Apoptosis
Cell Differentiation - drug effects
Cell Proliferation
Coculture Techniques
Insulin Receptor Substrate Proteins
Intracellular Signaling Peptides and Proteins
Keratinocytes - cytology
Keratinocytes - drug effects
Keratinocytes - metabolism
Mice
Mice, Knockout
Mitogen-Activated Protein Kinases - metabolism
Models, Biological
Oncogene Protein v-akt - metabolism
Phosphatidylinositol 3-Kinases - metabolism
Phosphoproteins - metabolism
Protein Kinases - pharmacology
Receptor, IGF Type 1 - deficiency
Receptor, IGF Type 1 - metabolism
Signal Transduction
Skin - cytology
Skin - growth & development
TOR Serine-Threonine Kinases
Online AccessGet full text

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Abstract Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
AbstractList The insulin-like growth factor 1 receptor (IGF-1R) is a multifunctional receptor that mediates signals for cell proliferation, differentiation, and survival. Genetic experiments showed that IGF-1R inactivation in skin results in a disrupted epidermis. However, because IGF-1R-null mice die at birth, it is difficult to study the effects of IGF-1R on skin. By using a combined approach of conditional gene ablation and a three-dimensional organotypic model, we demonstrate that IGF-1R-deficient skin cocultures show abnormal maturation and differentiation patterns. Furthermore, IGF-1R-null keratinocytes exhibit accelerated differentiation and decreased proliferation. Investigating the signaling pathway downstream of IGF-1R reveals that insulin receptor substrate 2 (IRS-2) overexpression compensates for the lack of IGF-1R, whereas IRS-1 overexpression does not. We also demonstrate that phosphatidylinositol 3-kinase and extracellular signal-regulated kinase 1 and 2 are involved in the regulation of skin keratinocyte differentiation and take some part in mediating the inhibitory signal of IGF-1R on differentiation. In addition, we show that mammalian target of rapamycin plays a specific role in mediating IGF-1R impedance of action on keratinocyte differentiation. In conclusion, these results reveal that IGF-1R plays an inhibitory role in the regulation of skin development and differentiation.
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
Author Derek LeRoith
Martin Holzenberger
Galina Weingarten
Dirk Breitkreutz
Marianna Sadagurski
Efrat Wertheimer
Christopher J. Rhodes
Shoshana Yakar
AuthorAffiliation Department of Pathology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel, 1 Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, 2 INSERM U515, Saint-Antoine Hospital, Paris, France, 3 Pacific Northwest Research Institute, Seattle, Washington, 4 German Cancer Research Center, Division A080, Heidelberg, Germany 5
AuthorAffiliation_xml – name: Department of Pathology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel, 1 Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, 2 INSERM U515, Saint-Antoine Hospital, Paris, France, 3 Pacific Northwest Research Institute, Seattle, Washington, 4 German Cancer Research Center, Division A080, Heidelberg, Germany 5
Author_xml – sequence: 1
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  fullname: Wertheimer, Efrat
  email: effy@patholog.tau.ac.il
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/16537911$$D View this record in MEDLINE/PubMed
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Corresponding author. Mailing address: Department of Pathology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. Phone: 972-3-640-6111. Fax: 972-3-640-9141. E-mail: effy@patholog.tau.ac.il.
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The insulin-like growth factor 1 receptor (IGF-1R) is a multifunctional receptor that mediates signals for cell proliferation, differentiation, and survival....
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SubjectTerms Animals
Apoptosis
Cell Differentiation - drug effects
Cell Proliferation
Coculture Techniques
Insulin Receptor Substrate Proteins
Intracellular Signaling Peptides and Proteins
Keratinocytes - cytology
Keratinocytes - drug effects
Keratinocytes - metabolism
Mice
Mice, Knockout
Mitogen-Activated Protein Kinases - metabolism
Models, Biological
Oncogene Protein v-akt - metabolism
Phosphatidylinositol 3-Kinases - metabolism
Phosphoproteins - metabolism
Protein Kinases - pharmacology
Receptor, IGF Type 1 - deficiency
Receptor, IGF Type 1 - metabolism
Signal Transduction
Skin - cytology
Skin - growth & development
TOR Serine-Threonine Kinases
Title Insulin-Like Growth Factor 1 Receptor Signaling Regulates Skin Development and Inhibits Skin Keratinocyte Differentiation
URI http://mcb.asm.org/content/26/7/2675.abstract
https://www.tandfonline.com/doi/abs/10.1128/MCB.26.7.2675-2687.2006
https://www.ncbi.nlm.nih.gov/pubmed/16537911
https://search.proquest.com/docview/17093118
https://search.proquest.com/docview/67757482
https://pubmed.ncbi.nlm.nih.gov/PMC1430337
Volume 26
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