CNTF receptor α mRNA expression in rodent cell lines and developing rat
Ciliary neurotrophic factor (CNTF) has been shown to modulate the in vitro and in vivo survival, proliferation and differentiation of many neuronal cell types. Evidence indicates that it produces most if not all these effects by binding to a receptor subunit referred to as the CNTF receptor α compon...
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Published in | Brain research. Molecular brain research. Vol. 25; no. 3; pp. 251 - 256 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier B.V
01.09.1994
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Subjects | |
Online Access | Get full text |
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Summary: | Ciliary neurotrophic factor (CNTF) has been shown to modulate the in vitro and in vivo survival, proliferation and differentiation of many neuronal cell types. Evidence indicates that it produces most if not all these effects by binding to a receptor subunit referred to as the CNTF receptor α component (CNTFRα). We cloned a cDNA encoding part of the rat CNTFRα and used it in Northern analyses to study CNTFRα mRNA expression. Examination of various tissues of embryonic day 18 and postnatal day 14 rats indicated that CNTFRα mRNA is primarily but not exclusively expressed in brain at these stages of development. Further studies revealed that the CNTFRα transcripts are present throughout brain development from embryonic day 12 to adulthood and display a widespread distribution in the adult brain. A survey of rodent cell lines detected highest CNTFRα mRNA concentrations in neuronal lines and a low concentration in a Schwann cell derived line. CNTFRα mRNA was not detected in fibroblast lines and a glioma line. Finally, nerve growth factor treatment decreased CNTFRα mRNA levels in PC12 cells. This result demonstrates that signal transduction processes activated by a neurotrophin can influence CNTF activated signal transduction processes. Such cross-talk may play an important in vivo role in the development and maintenance of the many neuronal cell types that are responsive to both neurotrophins and CNTF. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0169-328X 1872-6941 |
DOI: | 10.1016/0169-328X(94)90160-0 |