Abstract
The rotavirus nonstructural glycoprotein NSP4 is an intracellular receptor that mediates the acquisition of a transient membrane envelope as subviral particles bud into the endoplasmic reticulum. NSP4 also causes an increase in intracellular calcium in insect cells. Purified NSP4 or a peptide corresponding to NSP4 residues 114 to 135 induced diarrhea in young (6 to 10 days old) CD1 mice. This disease response was age-dependent, dose-dependent, and specific. Electrophysiologic data from intestinal mucosa showed that the NSP4 114-135 peptide potentiates chloride secretion by a calcium-dependent signaling pathway. Diarrhea is induced when NSP4, acting as a viral enterotoxin, triggers a signal transduction pathway.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Aging*
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Amino Acid Sequence
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Animals
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Calcium / metabolism
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Carbachol / pharmacology
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Chlorides / metabolism
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Colforsin / pharmacology
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Diarrhea / etiology*
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Diarrhea / prevention & control
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Diarrhea / virology
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Enterotoxins / toxicity*
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Glycoproteins / immunology
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Glycoproteins / toxicity*
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Immune Sera / administration & dosage
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Immunization
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In Vitro Techniques
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Intestinal Mucosa / drug effects
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Intestinal Mucosa / metabolism
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Mice
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Molecular Sequence Data
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Peptide Fragments / toxicity
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Receptors, Virus
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Rotavirus / pathogenicity*
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Rotavirus Infections / prevention & control
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Rotavirus Infections / virology*
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Signal Transduction
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Toxins, Biological
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Viral Nonstructural Proteins / immunology
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Viral Nonstructural Proteins / toxicity*
Substances
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Chlorides
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Enterotoxins
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Glycoproteins
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Immune Sera
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NS28 protein, rotavirus
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Peptide Fragments
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Receptors, Virus
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Toxins, Biological
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Viral Nonstructural Proteins
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Colforsin
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Carbachol
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Calcium