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  Acetylcholine receptor gene expression in experimental autoimmune myasthenia gravis

Asher, O., Neumann, D., Witzemann, V., & Fuchs, S. (1990). Acetylcholine receptor gene expression in experimental autoimmune myasthenia gravis. FEBS Letters, 267(2), 231-235. doi:10.1016/0014-5793(90)80932-9.

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Item Permalink: https://hdl.handle.net/11858/00-001M-0000-0019-AD0A-1 Version Permalink: https://hdl.handle.net/21.11116/0000-0000-7D37-7
Genre: Journal Article

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FEBSLett_267_1990_231.pdf (Any fulltext), 527KB
 
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 Creators:
Asher, Orna, Author
Neumann, Drorit, Author
Witzemann, Veit1, 2, 3, 4, Author           
Fuchs, Sara, Author
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              
2Working Group Witzemann / Koenen, Max Planck Institute for Medical Research, Max Planck Society, ou_1497748              
3Molecular anatomy of the neuromuscular junction, Max Planck Institute for Medical Research, Max Planck Society, ou_1497727              
4Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              

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Free keywords: Adult and embryonic acetylcholine receptor; Experimental autoimmune myasthenia gravis; Subunit transcript
 Abstract: Acetylcholine receptor (AChR) gene expression was analyzed in experimental autoimmune myasthenia gravis (EAMG) in rabbits, rats and mice. An increase in AChR transcripts was demonstrated to be exclusively associated with myasthenic symptoms and with a severe loss in membrane AChR. An increase of alpha-, beta-, epsilon-, and delta-subunit specific mRNAs (5.2-, 1.6-, 3.2- and 3.7-fold, respectively), which code for the adult type of AChR (alpha 2 beta epsilon delta) was observed in EAMG in rats. The gamma-subunit transcript was not detectable in myasthenic or healthy rats. It appears that the regulatory control of AChR gene expression in EAMG is different from that observed upon denervation.

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Language(s): eng - English
 Dates: 1990-05-141990-07-16
 Publication Status: Issued
 Pages: 5
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.1016/0014-5793(90)80932-9
URI: https://www.ncbi.nlm.nih.gov/pubmed/2379584
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Title: FEBS Letters
  Other : FEBS Lett.
Source Genre: Journal
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Publ. Info: Amsterdam : Elsevier
Pages: - Volume / Issue: 267 (2) Sequence Number: - Start / End Page: 231 - 235 Identifier: ISSN: 0014-5793
CoNE: https://pure.mpg.de/cone/journals/resource/954925399501