M3 Muscarinic Acetylcholine Receptors Regulate Cytoplasmic Myosin ...

Clipboard, Search History, and several other advanced features are temporarily unavailable. Skip to main page content

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation Search: Search Advanced Clipboard Save Email Send to

• Clipboard
• My Bibliography
• Collections
• Citation manager

Display options Display options Format Abstract PubMed PMID

Save citation to file

Format: Summary (text) PubMed PMID Abstract (text) CSV Create file Cancel

Email citation

Email address has not been verified. Go to My NCBI account settings to confirm your email and then refresh this page. To: Subject: Body: Format: Summary Summary (text) Abstract Abstract (text) MeSH and other data Send email Cancel

Add to Collections

• Create a new collection
• Add to an existing collection

Name your collection: Name must be less than 100 characters Choose a collection: Unable to load your collection due to an error Please try again Add Cancel

Add to My Bibliography

• My Bibliography

Unable to load your delegates due to an error Please try again Add Cancel

Your saved search

Name of saved search: Search terms: Test search terms Would you like email updates of new search results? Saved Search Alert Radio Buttons

• Yes
• No

Email: (change) Frequency: Monthly Weekly Daily Which day? The first Sunday The first Monday The first Tuesday The first Wednesday The first Thursday The first Friday The first Saturday The first day The first weekday Which day? Sunday Monday Tuesday Wednesday Thursday Friday Saturday Report format: Summary Summary (text) Abstract Abstract (text) PubMed Send at most: 1 item 5 items 10 items 20 items 50 items 100 items 200 items Send even when there aren't any new results Optional text in email: Save Cancel

Create a file for external citation management software

Create file Cancel

Your RSS Feed

Name of RSS Feed: Number of items displayed: 5 10 15 20 50 100 Create RSS Cancel RSS Link Copy

Full text links

Elsevier Science Full text links

Actions

CiteCollectionsAdd to Collections

• Create a new collection
• Add to an existing collection

Name your collection: Name must be less than 100 characters Choose a collection: Unable to load your collection due to an errorPlease try again Add Cancel PermalinkPermalinkCopyDisplay options Display options Format AbstractPubMedPMID

Page navigation

• Title & authors
• Abstract
• MeSH terms
• Substances
• LinkOut - more resources

Title & authors Abstract MeSH terms Substances LinkOut - more resources Full text links CiteDisplay options Display options Format AbstractPubMedPMID

Abstract

Although muscarinic acetylcholine receptors (mAChR) regulate the activity of smooth muscle myosin, the effects of mAChR activation on cytoplasmic myosin have not been characterized. We found that activation of transfected human M3 mAChR induces the phosphorylation of myosin light chains (MLC) and the formation of myosin-containing stress fibers in Chinese hamster ovary (CHO-m3) cells. Direct activation of protein kinase C (PKC) with phorbol 12-myristate 13-acetate (PMA) also induces myosin light chain phosphorylation and myosin reorganization in CHO-m3 cells. Conventional (alpha), novel (delta), and atypical (iota) PKC isoforms are activated by mAChR stimulation or PMA treatment in CHO-m3 cells, as indicated by PKC translocation or degradation. mAChR-mediated myosin reorganization is abolished by inhibiting conventional PKC isoforms with Go6976 (IC50 = 0.4 microM), calphostin C (IC50 = 2.4 microM), or chelerythrine (IC50 = 8.0 microM). Stable expression of dominant negative RhoAAsn-19 diminishes, but does not abolish, mAChR-mediated myosin reorganization in the CHO-m3 cells. Similarly, mAChR-mediated myosin reorganization is diminished, but not abolished, in CHO-m3 cells which are multi-nucleate due to inactivation of Rho with C3 exoenzyme. Expression of dominant negative RhoAAsn-19 or inactivation of RhoA with C3 exoenzyme does not affect PMA-induced myosin reorganization. These findings indicate that the PKC-mediated pathway of myosin reorganization (induced either by M3 mAChR activation or PMA treatment) can continue to operate even when RhoA activity is diminished in CHO-m3 cells. Conventional PKC isoforms and RhoA may participate in separate but parallel pathways induced by M3 mAChR activation to regulate cytoplasmic myosin. Changes in cytoplasmic myosin elicited by M3 mAChR activation may contribute to the unique ability of these receptors to regulate cell morphology, adhesion, and proliferation.

PubMed Disclaimer

MeSH terms

• ADP Ribose Transferases / metabolism Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Animals Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Botulinum Toxins* Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• CHO Cells Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Carbachol / pharmacology Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Cricetinae Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Cytoplasm / metabolism Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• GTP-Binding Proteins / metabolism* Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Humans Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Isoenzymes / metabolism* Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Myosins / metabolism* Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Protein Kinase C / metabolism* Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Receptor, Muscarinic M1 Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Receptor, Muscarinic M3 Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Receptors, Muscarinic / metabolism* Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Tetradecanoylphorbol Acetate / pharmacology Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• rhoA GTP-Binding Protein Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search

Substances

• Isoenzymes Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Receptor, Muscarinic M1 Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Receptor, Muscarinic M3 Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Receptors, Muscarinic Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Carbachol Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• ADP Ribose Transferases Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• exoenzyme C3, Clostridium botulinum Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Protein Kinase C Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Botulinum Toxins Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• GTP-Binding Proteins Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Myosins Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• rhoA GTP-Binding Protein Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search
• Tetradecanoylphorbol Acetate Actions
  • Search in PubMed
  • Search in MeSH
  • Add to Search

LinkOut - more resources

• Full Text Sources

  • Elsevier Science

• Miscellaneous

  • NCI CPTAC Assay Portal

Full text links [x] Elsevier Science [x] Cite Copy Download .nbib .nbib Format: AMA APA MLA NLM Send To

• Clipboard
• Email
• Save
• My Bibliography
• Collections
• Citation Manager

[x]

NCBI Literature Resources

MeSH PMC Bookshelf Disclaimer

The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). Unauthorized use of these marks is strictly prohibited.