دورية أكاديمية

Insulin and IGF1 modulate turnover of polysialylated neural cell adhesion molecule (PSA-NCAM) in a process involving specific extracellular matrix components.

التفاصيل البيبلوغرافية
العنوان: Insulin and IGF1 modulate turnover of polysialylated neural cell adhesion molecule (PSA-NCAM) in a process involving specific extracellular matrix components.
المؤلفون: Monzo HJ; Faculty of Medical and Health Sciences, Centre for Brain Research, The University of Auckland, Auckland, New Zealand., Park TI, Dieriks BV, Jansson D, Faull RL, Dragunow M, Curtis MA
المصدر: Journal of neurochemistry [J Neurochem] 2013 Sep; Vol. 126 (6), pp. 758-70. Date of Electronic Publication: 2013 Aug 05.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Wiley on behalf of the International Society for Neurochemistry Country of Publication: England NLM ID: 2985190R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1471-4159 (Electronic) Linking ISSN: 00223042 NLM ISO Abbreviation: J Neurochem Subsets: MEDLINE
أسماء مطبوعة: Publication: 2001- : Oxford, UK : Wiley on behalf of the International Society for Neurochemistry
Original Publication: New York : Raven Press
مواضيع طبية MeSH: Extracellular Matrix/*metabolism , Hypoglycemic Agents/*pharmacology , Insulin/*pharmacology , Insulin-Like Growth Factor I/*pharmacology , Neural Cell Adhesion Molecules/*metabolism , Sialic Acids/*metabolism, Blotting, Western ; Calcium/metabolism ; Cell Line, Tumor ; Collagen Type IV/metabolism ; Endocytosis/drug effects ; Humans ; Image Processing, Computer-Assisted ; Immunohistochemistry ; Protein Processing, Post-Translational ; Real-Time Polymerase Chain Reaction
مستخلص: Cellular interactions mediated by the neural cell adhesion molecule (NCAM) are critical in cell migration, differentiation and plasticity. Switching of the NCAM-interaction mode, from adhesion to signalling, is determined by NCAM carrying a particular post-translational modification, polysialic acid (PSA). Regulation of cell-surface PSA-NCAM is traditionally viewed as a direct consequence of polysialyltransferase activity. Taking advantage of the polysialyltransferase Ca²⁺-dependent activity, we demonstrate in TE671 cells that downregulation of PSA-NCAM synthesis constitutes a necessary but not sufficient condition to reduce cell-surface PSA-NCAM; instead, PSA-NCAM turnover required internalization of the molecule into the cytosol. PSA-NCAM internalization was specifically triggered by collagen in the extracellular matrix (ECM) and prevented by insulin-like growth factor (IGF1) and insulin. Our results pose a novel role for IGF1 and insulin in controlling cell migration through modulation of PSA-NCAM turnover at the cell surface. Neural cell adhesion molecules (NCAMs) are critically involved in cell differentiation and migration. Polysialylation (PSA)/desialylation of NCAMs switches their functional interaction mode and, in turn, migration and differentiation. We have found that the desialylation process of PSA-NCAM occurs via endocytosis, induced by collagen-IV and blocked by insulin-like growth factor (IGF1) and insulin, suggesting a novel association between PSA-NCAM, IGF1/insulin and brain/tumour plasticity.
(© 2013 International Society for Neurochemistry.)
فهرسة مساهمة: Keywords: IGF1; PSA-NCAM; extracellular matrix; insulin; migration
المشرفين على المادة: 0 (Collagen Type IV)
0 (Hypoglycemic Agents)
0 (Insulin)
0 (Neural Cell Adhesion Molecules)
0 (Sialic Acids)
0 (polysialic acid)
67763-96-6 (Insulin-Like Growth Factor I)
SY7Q814VUP (Calcium)
تواريخ الأحداث: Date Created: 20130713 Date Completed: 20131031 Latest Revision: 20131121
رمز التحديث: 20221213
DOI: 10.1111/jnc.12363
PMID: 23844825
قاعدة البيانات: MEDLINE
الوصف
تدمد:1471-4159
DOI:10.1111/jnc.12363